HE EFFEGTE QF EXOGENOUS- ,3“

 

 

~ 1974

 
    
   

  

LIBRARY

Michigan State
University

TN EEIE

 

ABS TRAC T

THE EFFECTS OF EXOGENOUS ALDOSTERONE
AND CORTICOSTERONE ON RENAL FUNCTION
IN THE ADULT MALE DOMESTIC CHICKEN
(Gallus domesticus)

 

BY

Edward A. Cogger
i

Two experiments were conducted to determine the

effects of exogenous administration of the two primary avian

 

adrenocortical steroids on renal function in the adult male
chicken. The steroids administered were corticosterone (a
glucocorticoid) and aldosterone (a mineralocorticoid). The
method, duration, and quantity of administration were varied in
the two experiments. Urine was collected in these experiments
from anesthetized (sodium phenobarbital) roosters by a technique
which surgically modifies the cloaca to separate urine and feces,
‘ and is only useful for acute collections.

In the first experiment, corticosterone (3. 0, 6. O,
9. O, and 12. O Pg/min) and aldosterone (0. O4, 0. 08, 0. 12, and
O. 16 Pg/min) were infused for 95 minutes and during this time

plasma concentration of sodium (PNa) and potassium (PK),

 

glomerular filtration rate (GFR), urine flow rate (V), and excre-
tion rates of sodium (ENa) and potassium (EK) in the liquid phase

of the urine were monitored in nine 10 minute periods. PNa

Edward A. Cogger
remained stable for the duration of the experiment. Though PK
showed greater variability than PNa’ this was not related to the
steroid treatments. GFR was not affected by aldosterone but
there was a significant (p <. 05) interaction between level and
time when corticosterone was infused. At 6. O and 9. Dug/min
GFR increased by O. 44 (p < . 10) and 0. 78 (p <. 05) ml/min/kg,
respectively, after 55-75 minutes of infusion but waned during
the 75-95 minute period. The aldosterone treatments had no
effect on V or percent water reabsorbed (Reab H20) but there
was an experiment-wide time effect (p< . 05). V remained
stable up to 50 minutes (23. Spl/min/kg) during infusion then
began to increase until the end of the experiment (28. 4pl/min/
kg). This was accompanied by a decrease in Reab H20 (98. 34%
to 97. 90%). Corticosterone at 9. 0 and 12. O g/min caused sig-
nificant (p < . 05) increases in V by 55-75 minutes and 30-50
minutes, respectively. The diuresis at the 9. Dug/min treatment
(from 18. 4 to 41. 9pl/min/kg) was the result of the change in
GFR exhibited by this group whereas the diuresis seen in the
12. O g/min treatment (from 29.1 to 81. 4pl/min/kg) was related
to a decrease in Reab HzO'

Corticosterone at 3. O, 6. O, and 9. O pg/min caused
significant (p <. 05) increases in ENa by 55-75 minutes (. 99, . 75,
and . 87peq/min/kg) which declined during the 75-95 minute

period. When the excretion rate was expressed as a percent of

 

 

 

 

 

Edward A. Cogger
the filtered load of sodium only the 3. O rug/min treatment showed
a significant (p <. 05) increase in excretion (from O. 33 to O. 81%
by 55. 75 minutes). There was no effect by any treatment level
on the EK which did rise (from O. 81 to l. 04peq/min/kg) signifi-
cantly (p <. 05) on an experiment-wide basis.

Aldosterone at the doses given did not affect the ENa
during the 95 minutes of infusion but EK was significantly affected
(p <. 05). Aldosterone at O. 08 and O. 12 Pg/min exhibited con-
trasting actions. The former increased EK by . 42 Peq/min/kg
whereas the latter decreased EK by . 48 peq/min/kg at 55-75
minutes. EK was returning toward initial values when the
experiment was terminated. The clearance of potassium (CK)
followed the same trend at 0. 08 pg/min, however at O. 12 pg/min
it remained depressed until the end of the experiment. When
expressed as percent of filtered load no significant effects on
potassium excretion were observed.

In the second experiment, the male chickens
received either 14. 0 mg/kg/day of corticosterone in stabilized
suspension (0. 9% saline with 1% methyl cellulose), O. 35 mg/kg/
day of aldosterone in safflower oil, or one of the carrier sub-
stances. At the end of three days of treatment urine was
collected for a 30 minute period. Sodium and potassium excre-
tion rates were measured in the liquid and solid phases of the

urine. A significant (p <. 01) diuresis was observed in the

 

 

 

 

 

 

Edward A. Cogger
corticosterone treated birds (76. 2 in contrast to 12. 4pl/min/kg).
This was accompanied by a significant decrease in water
resorption (p <. 01) and body weight (p <. 05).

Aldosterone and corticosterone significantly
depressed the sodium excretion rate in liquid, solid and total
urine. The total excretory rates of sodium were 82. 3 1' 24. 4
(SD), 36. 5 i 3. 6, and 27. 1 2 9. Opeq/3O min/kg for control,
corticosterone, and aldosterone treated birds, respectively.

Corticosterone caused a significant (p < . 01) increase in the

 

excretion rate of potassium in liquid and total urine while
aldosterone had no effect. The excretion rate of potassium in
the solid urine was unaffected by the steroids. The potassium
excretory rates in total urine were 40. 6 1’ l7. 5 (SD), 103. 9 i

27. l, and 36. 5 1 l3. 3peq/3O min/kg for control, corticosterone,
and aldosterone treated birds, respectively.

The percent of sodium and potassium excreted in
solid urine was significantly (p <. 01) reduced by corticosterone
(sodium, 15. 2% versus 3. 7%; potassium, 39. 2% versus 11.1%).
This lowered percentwise excretion of the sodium and potassium

may be indicative of increased excretion of hydrogen or

 

ammonium ions, which have a higher affinity for urate.

 

 

 

 

THE EFFECTS OF EXOGENOUS ALDOSTERONE

AND CORTICOSTERONE ON RENAL FUNCTION

IN THE ADULT MALE DOMESTIC CHICKEN
(Gallus domesticus)

 

by

Edward Arnold Cogger

A THESIS

Submitted to
Michigan State University
in partial fulfillment of the requirements
for the degree of

DOCTOR OF PHILOSOPHY

Department of Poultry Science

1974

ACKNOWLEDGEMENTS

I would like to thank the many people who have been
or are associated with Michigan State University and the
Department of Poultry Science without whose encouragement
and/or assistance this dissertation may not have been possible.
The following list which is neither complete nor necessarily in
order of importance represents those whom come first to my
mind: Dr. R. K. Ringer, Dr. T. Coleman, Ms. Sue Asher,
Mr. R. Jacobs, Dr. R. Bayer, Dr. S. Iturri, Dr. C. Knight,
Dr. D. Polin, Dr. E. P. Rienede, Dr. B. Selleck and Dr. H. C.
Zindel.

I also wish to extend my deepest gratitude to my
family for their encouragement throughout the years and without
whom this would not have been possible. To Pat, Charlie, Jeni,
Mom, Dad, Phil, Judy and Adelle words cannot express my
thanks and love. Lastly to Henry Ford Carr, my wife's father
who treated me as a son but whose death deprived us of his joy

at the final celebration, thank you.

ii

INTRODUC TION

OBJECTIVES

TABLE OF CONTENTS

REVIEW OF LITERATURE

The Urinary Apparatus

Gross structure . . . . . . .

The nephrons and their organization .......... . .

The blood supply . . . . . . .
Methods of Collecting Avian Urine

Avian Renal Function . . . .

The elements of renal function

Renal response to osmotic challenge . . . . . . . . . . . .

The role of the adrenal

The role of the neurohypophysis . . . . . . . ...... . . .

Other considerations . . . . .

The Cloaca, Colon, and Ceca

MATERIALS AND METHODS

Experiment 1

Experiment 2

0000......

iii

11

ll

l4

19

26

27

28

30

3O

39

iv

Statistical Analyses . . . . ...... . ....... . . ........... 42
RESULTS AND DISCUSSION . . ..... . . . . ..... . . . . . . . . . 44
Plasma Sodium and Potassium ....... . ............. 44
Glomerular Filtration Rate (GFR) .................. 49
TubularFunction ....... ...... 54
Urine flow and water reabsorption . . . .......... . . 54
Sodium and potassium excretion . . . .............. 67
CONCLUSIONS ..... ........... 85

LITERATURE CITED 00.0.0...OOOOOOOOOOOOOOOOOOOOOOO 87

 

APPENDIX OOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOO 101

 

Table

LIS T OF TABLES

Composition of Bray's Solution ............
Parameters Measured in Experiments 1 and 2

Analysis of Variance Table for Selected
Parameters Measured in Experiment 1

from Corticosterone Treated Adult

Male Chickens ........

Analysis of Variance Table for Selected
Parameters Measured in Experiment 1

from Aldosterone Treated Adult Male
Chickens . .....

Analysis of Variance Table for Selected
Parameters Measured in Experiment 2 . . . . . .

The Effects of Corticosterone Infusion
Rate on Glomerular Filtration Rate for
95 Minutes GFR (ml/min/kg) Corticosterone .

The Effects of Aldosterone Infusion

Rate on Glomerular Filtration Rate

for 95 Minutes GFR (ml/min/kg)

Aldosterone ..... . ......

The Effects of Aldosterone (. 35 mg/kg/day)
and Corticosterone (14. 0 mg/kg/day)
Administered for Three Days on Glomerular
Filtration Rate, Urine Flow Rate, Water
Resorption, Urate Excretion Rate, and

Body Weight Changes . . . ....... . .........

V

Page
35

38

52

58

59

6O

61

 

Table

10.

ll.

12.

l3.

14.

15.

16.

17.

18.

The Effects of Corticosterone Infusion
Rate on Urine Flow Rate for 95 Minutes

V (Fl/min/kg) Corticosterone . . . . . . . . . . . . . .

The Effects of Corticosterone Infusion
Rate on Water Resorption for 95

Minutes Reab H20 (‘70) Corticosterone .......

The Effects of AldosteroneInfusion
Rate on Urine Flow Rate for 95

Minutes V (Fl/min/kg) Aldosterone .........

The Effects of Aldosterone Infusion
Rate on Water Resorption for 95

Minutes Reab H20 (‘70) Aldosterone . . . . . . . . .

The Effects of Corticosterone Infusion
Rate on the Excretion Rate of Sodium
for 95 Minutes ENa (Peq/min/kg)

Corticosterone . . . . . . . . . . . ................

The Effects of Corticosterone Infusion
Rate on the Clearance of Sodium for

95 Minutes CNa (”l/min/kg) Corticosterone . .

The Effects of Corticosterone Infusion
Rate on the Percent of Filtered Sodium
Excreted for 95 Minutes %ENa

Corticosterone ..........

The Effects of Aldosterone Infusion
Rate on the Excretion Rate of Sodium
for 95 Minutes ENa (peq/min/kg)

Aldosterone .................. ...........

The Effects of Aldosterone Infusion
Rate on the Clearance of Sodium for

95 Minutes CNa (Pl/min/kg) Aldosterone . . . .

The Effects of Aldosterone Infusion
Rate on the Percent of Filtered Sodium
Excreted for 95 Minutes ”/oENa

Aldosterone.................. ........

Page

63

64

65

66

68

69

7O

74

75

75

Table

19.

20.

21.

22.

23.

24.

25.

26.

vii
Page

The Effects of Aldosterone (O. 35 mg/kg/day)

and Corticosterone (l4. 0 mg/kg/day)

Administered for 3 days on the Excretion

Rates of Sodium and Potassium in Liquid,

Solid and Total Urine, and Liquid Urine
Concentration of Sodium and Potassium ....... 76

The Effects of Corticosterone Infusion

Rate on the Excretion Rate of Potassium

for 95 Minutes EK (Feq/min/kg)

Corticosterone ...... . . . . . ................. 77

The Effects of Corticosterone Infusion
Rate on the Clearance of Potassium for
95 Minutes CK (pl/min/kg) Corticosterone . . . . 78

The Effects of Corticosterone Infusion

Rate on the Percent of Filtered

Potassium Excreted for 95 Minutes

%EK Corticosterone . . . . . . . . ............... 78

The Effects of Aldosterone Infusion

Rate on the Excretion Rate of

Potassium for 95 Minutes EK

(peq/min/kg) Aldosterone ......... . . . . . . . . . 80

The Effects of Aldosterone Infusion

Rate on the Clearance of Potassium

for 95 Minutes CK (pl/min/kg)

Aldosterone ...... ........ ...... 83

The Effects of Aldosterone Infusion

Rate on the Percent of Filtered

Potassium Excreted for 95 Minutes

%EK Aldosterone . . . ........ . . . . . ......... 84

The Effects of Aldosterone (O. 35 mg/

kg/day) and Corticosterone (14. 0 mg/

kg/day) Administered for 3 Days on

Percent of Total Sodium and Potassium

Excreted in Solid Urine ......... . . . . . . . . . . . 84

Figure

LIST OF FIGURES

Biochemical pathways of
steroidogenesis in the
class Aves

Plasma sodium concentrations
during the 95 minutes of
corticosterone infusion . . . . . . . . . . . .

Plasma sodium concentrations
during the 95 minutes of
aldosterone infusion . . . . . . . . . . . . . . .

Plasma potassium concentrations
during the 95 minutes of
corticosterone infusion . . . . . . . . . . . .

Plasma potassium concentrations
during the 95 minutes of
aldosterone infusion

Mean plasma potassium
concentrations of all roosters
in Experiment 1

The effect of corticosterone
infusion rates on mean changes
in glomerular filtration rate at

55-75 minutes from 0-30 minutes . . . . .

Relationship between urine flow
rate and water resorption in
control and corticosterone treated

roosters in Experiment 1 . . . . . . . . . . . .

viii

00......

Page

21

45

46

47

48

50

53

55

 

 

Figure

Page

Relationship between urine flow
rate and water resorption in
control, aldosterone and
corticosterone treated roosters

inEXperimentZ 00.0.0.0..OOOOOOOOOOOOOOOO 57

IN TRODUC TION

The avian kidney is an intriguing organ anatomically
and physiologically. It has three types of nephrons: those with
loops of Henle (like mammalian nephrons), those with short
100ps which are anatomically different from the 100ps of Henle,
and those with no 100ps of Henle (like the reptilian nephron).
These are arranged in the multilobar organ in many separate
medullary, and their associated cortical, lobules. In addition to
the arterial blood supply, there is a functional venous portal
system routing blood to the peritubular capillaries. The renal
portal valve is strategically located so it can control the flow of
blood into the portal system.

The kidney of birds has limited concentrating ability.
The domestic chicken will excrete urine only twice as concen-
trated osmotically as plasma under dehydrating conditions; some
other birds can excrete urines with four-five fold osmotic con—
centrations. However, the bird excretes its nitrogenous waste
as uric acid rather than urea; the uric acid precipitates in the
urine and becomes osmotically inactive. The uric acid precipi—

tate is arranged in irregular layers trapping soluble matter

1

which contains significant quantities of sodium and potassium.
This further reduces the osmolality of the liquid urine. Many
birds which are adapted to marine environments possess func-
tional salt secreting organs in addition to the kidney. Also,
significant post-renal modifications of the urine occur in the
cloaca, colon, and/or ceca of birds.

Renal studies of electrolyte and water excretion in
birds have been conducted primarily with species adapted to
marine and arid environments. Most studies have involved salt
loading, water loading, and/or dehydration. In general the role
of the adrenal steroid hormones in salt and water metabolism
has been little studied in birds and less so in the domestic
chicken. The research reported herein was undertaken to study
the role of the primary avian adrenal steroids on renal function

in the domestic chicken.

OBJECTIVES

1. To ascertain the effects of the primary avian
adrenal steroid hormones, aldosterone and corticosterone, on
renal function in the adult male chicken.

2. To determine if the excretion of sodium and
potassium in liquid urine is indicative of their excretion in total
urine.

3. To develOp a technique for acute collection of

urine in the adult male chicken.

REVIEW OF LITERATURE

The Urinary Apparatus

 

Gross structure

 

The avian kidneys are paired organs which lie
ventrolateral to the vertebral column within the boney depression
of the pelvis. They are relatively large organs ranging from 1. 0
to 2.6 (Benoit, 1950 as cited by Sturkie, 1965) and 0. 6 to 2. 1
(Johnson, 1968) percent of the body weight. Johnson (1968)
observed an inverse relationship between the relative kidney size
and body weight which was attributed to metabolic needs. No sex

difference was observed. In the chicken (Callus domesticus) the

 

kidney is divided into anterior, middle, and posterior divisions
(Goodchild, 1956 as cited by Siller and Hindle, 1969) which are
not related to the internal morphology (Siller and Hindle, 1969).
The ureters transport the urine from the kidney to the urodeum
of the cloaca. In the chicken, no bladder is present.

The nephrons and their organization

 

The avian kidney is a multilobar organ, but there is
disagreement in the literature as to what constitutes a lobe.

Since the avian ureteral-collecting duct complex is a continuous

4

dendritic system, analogies to the mammalian renal pelvis are
difficult to make. Johnson and Mugaas (1970b) considered a lobe
to be one medullary lobule and its peripheral cortical lobules,
whereas Siller and Hindle (1969) considered it to be the complex
of medullary lobules and their associated cortical lobules drained
by a single uretral branch. In the chicken, Siller and Hindle
(1969) found a single cortical lobule for each medullary lobule;
this was rare among other species (Johnson and Mugaas, 1970b).
The cortical lobule is bounded by the afferent inter-
lobular veins of the renal portal system (see below) and has a
central efferent intralobular vein with the proximal convoluted
tubules central to the glomeruli, and distal convoluted tubules
and collecting ducts peripheral to the glomeruli (Spanner, 1925;
Siller and Hindle, 1969; Siller, 1971). The medullary lobule is
an aggregation of the thick and thin segments of the 100ps of
Henle from the juxtamedullary nephrons, the collecting ducts,
and a vasa recta (Spanner, 1925; Sperber, 1948; Siller and
Hindle, 1969; Johnson and Mugaas, 1970b; Siller, 1971).
Poulson (1965) demonstrated a relationship between the numbers
of 100ps of Henle and the ability to concentrate urine in some
passerines. This finding was supported by Johnson and Mugaas
(1970a) and extended to implicate length of the 100ps of Henle and
interlobular association of the medullae. These observations

suggest a countercurrent multiplier system in passerines which

has been demonstrated in chickens and turkeys (Skadhauge and
Schmidt-Nielsen, 1967b).

Huber (1917) described three types of nephrons in the
avian kidney and a comprehensive description of their structure
was presented by Siller (1971). The most abundant type is the
cortical (reptilian) nephron which consists of a glomerulus, a
proximal and distral convoluted tubule, and a collecting duct.
The juxtamedullary (mammalian) nephron also contains a 100p of
Henle which extends into the medullary lobule. The third is an
intermediate type with a short medullary 100p unlike the loop of
Henle.

The glomeruli in birds are smaller and simpler than
mammalian glomeruli. They consist of a few (sometimes only
one) capillary 100ps surrounding a mass of mesangial cells
(Siller and Hindle, 1969). The ultrastructure of the avian
glomerulus compares to that of mammals with the exception of a
central mass of mesangial cells (Siller, 1971). A juxtaglomeru-
1ar apparatus has been described by several authors (Edwards,
1940; Smith, 1966; Sokabe _e_t_a_1. , 1969; Capelli e_ta_1. , 1970;
Siller, 1971).

The blood supply

 

There are three renal arteries to each kidney of the
domestic chicken. The anterior renal artery originates on the

aorta and supplies blood to the adrenal, testes or ovary, and the

7
anterior division of the kidney. The middle and posterior renal
arteries arise together from the sciatic artery and supply blood
to the middle and posterior division of the kidney (Siller and
Hindle, 1969). Sperber (1948) reported similar findings but also
stated that one or more fine branches to the kidney originate from
the femoral artery. Siller and Hindle (1969) were unable to con-
firm this finding. As the renal arteries ramify the renal tissue
their branches appear to follow the efferent veins; and the intra-

lobular arteries to each lobule originate from one or more of

 

these branches (Sperber, 1948; Siller and Hindle, 1969). The
intralobular arteries are arranged symmetrically around the
central vein of the lobule. The intralobular artery gives off
afferent arterioles that are directed toward the periphery of the
lobule and break up into the capillaries of the glomeruli. The
efferent arteriole is also directed toward the periphery and
enters the peritubular capillaries against the flow of the renal

portal blood (Sperber, 1948; Siller and Hindle, 1969).

 

The kidney of birds has a renal portal system. The

renal portal system supplies venous blood to the anterior, middle, :

 

and posterior divisions of the kidney and its capability of func—

tioning has been demonstrated (Sperber, 1946, 1948, 1960). The

t"-

caudal and cranial renal portal veins originate on the external
iliac vein (femoral vein) between the point where it enters the

body cavity and the renal portal valve. They supply the middle

8
and posterior lobes, and anterior lobe, respectively (Sperber,
1948; Akester, 1964). The cranial renal portal vein was shown
to be continuous with the vertebral venous sinuses (Akester,
1967a) and to give rise to the interlobular veins of the kidney's
anterior division (Sperber, 1948). The caudal renal portal vein
courses caudally through the renal tissue. The sciatic vein
joins it between the middle and posterior divisions of the kidney.
The caudal renal portal veins from an anastomosis with the
hypogastric veins from the tail region and the coccygeomesen-
teric vein (Sperber, 1948; Akester, 1964). The caudal renal
portal vein gives rise to the interlobular veins of the kidney's
middle and posterior division (Sperber, 1948). The interlobular
veins are continuous with the peritubular capillaries which are
drained by the intralobular or central vein (Sperber, 1948;
Akester, 1964; Siller and Hindle, 1969). The intralobular veins
leave the lobule and eventually drain into the anterior and
posterior renal veins. These veins form an anastomosis with
the external iliac vein just downstream from the renal portal
valve and the large vein formed unites with the vein from the
contralateral side to form the posterior vena cava (Sperber, 1948;
Akester, 1964). The location of the renal portal valve suggests
that it can control the flow of venous blood to the kidney or away
from the kidney to the heart. Physiological evidence for this

possibility was suggested by Sperber (1948), Rennick and Gandia

9
(1954), and Akester (1964,1967).

Methods 91 Collecting Avian Urine

 

The collection of avian urine is complicated by its
mixing with the feces in the cloaca. A number of techniques for
obtaining ureteral urine have been described in the literature and
no single procedure seems applicable to all needs. These
procedures fall into five general categories.

Two of those are best adapted to chronic studies,
particularly nutritional experiments. The first is the colostomy
described by Weiner (1902) and subsequently used by many inves-
tigators. This involves the formation of an artificial anus in the
abdominal wall. Procedures for exteriorization of the ureteral
Openings have been described by Hester _e_t§._l_. (1940), Hart and
Essex (1942), and Dixon and Wilkinson (1957). Though these
differ in specific surgical details they all involve reconstruction
of the cloaca such that the ureteral Openings are moved dorsally
to the base of the pygostyle. Both colostomy and exteriorization
of the ureters involve considerable postoperative care to remain
functional (Sperber, 1960) and in the case of colostomy intestinal
tonus problems are evident (Hart and Essex, 1942). At least in
one instance (Hart and Essex, 1942) after colostomy and exter-
iorization of the ureteral Openings one percent NaCl had to be
added to the diet to maintain viability of the birds. One modifi-

cation of the Dixon and Wilkinson procedure was claimed to have

10
overcome the problems of cloacal fistulation and wound
dehiscence (Elliott and Furneaux, 1971). Since the cloaca and
rectum seem to be involved in final urine modification (to be
discussed below), renal clearance studies after chronic use of
these techniques is questionable (Sykes, 1971).

Techniques for acute collection of avian urine can be
divided into three categories. The first is direct cannulation of
the ureters (Sharpe, 1912) which is accompanied by a diuresis
for at least thirty minutes (Hester _e_t_a_l_. , 1940). These cannulas
tend to become clogged with urates. The second is a funnel
technique which has many variations. Davis (1927) restrained
the bird on its back with the head tilted upward and used a large
catheter to drain the cloaca near the ureteral Openings. The
birds were starved and water loaded, but occasionally the rectum
had to be plugged with cotton to prevent contamination. This was
modified by Hart and Essex (1942) using a glass cannula with a
glass ball which fit in the rectum, positioning the cannula Open-
ing under the ureteral Openings allowing the bird to remain in the
upright position. Another modification (Bokori, 1961 as cited by
Sykes, 1971) used a dual cannula Open to the rectum and the
ureters. An initial diuresis normally occurs from the physical
handling of the bird when using this type of technique (Hester _ei
fl. , 1940; Hart and Essex, 1942).

The third technique was originally developed by

 

 

ll
Sperber (1946, 1948) to investigate the existence of a functional
renal portal system in the chicken. He simply sutured a small
funnel which was fitted with a separate larger collar over the
ureteral Openings. Because of the highly viscous nature of
avian urine, this was subsequently modified by perfusing the
funnels with a rinsing solution to prevent clogging (Lindahl and
Sperber, 1956; Campbell, 1960). This method has been widely
used particularly where collection from the separate kidneys is
required.

Avian Renal Function

 

The elements 9_f_ renal function

 

 

Cuypers (1959) demonstrated that glomerular
filtration is essential to urine formation in the chicken. He
showed that urine flow ceased after interruption of the arterial
blood supply to the kidney even though the renal portal system
was intact. The glomerular filtration rate (GFR) is central to
the study of renal function. Evidence suggests that the clearance
of inulin, a fructose polysaccharide, meets the criteria for
measuring GFR, i. e. , it is (l) freely filterable through the
glomerular capillary membrane, (2) biologically inert and
neither reabsorbed nor secreted by the nephron, (3) nontoxic and
does not alter renal function, and (4) quantifiable in plasma and
urine (Pitts, 1963). The ratio of inulin clearance to glucose

clearance in the chicken is equal to l. 01 after phlorizin

12
treatment (Pitts, 1938). GFR has been reported by various
authors to range between approximately one to three milliliters
per kilogram body weight per minute in the chicken (see Pitts,
1938; Korr, 1939; Sperber, 1960; Dantzler, 1966; Skadhauge,
1964; Skadhauge and Schmidt-Nielsen, 1967a). Large variations
in GFR have been reported within and among chickens (Langford
and Fallis, 1966). In the chick, GFR increases at hatching and
attains adult levels at nine days of age (Cooke and Young, 1970).

In other birds, the budgerygah (Krag and Skadhauge, 1972) and

 

the duck (Holmes, 1965; Holmes eta—1. , 1968) have GFR's of
slightly less than four and more than two milliliters per
kilogram per minute, respectively.

Tubular reabsorption occurs in the avian kidney.
One Of the most conspicuous examples of this is water. In the
chicken as much as 99 percent of filtered water can be reabsorbed
(Skadhauge and Schmidt—Nielsen, 1967a) whereas in the budgery-
gah, an inhabitant of arid areas, even greater reabsorption of
water can occur (Krag and Skadhauge, 1972). Tubular reab-
sorption of a solute is said to have occurred when its clearance
is less than the clearance of inulin (GFR). Pitts and Kerr (1938)
and Korr (1939) studied the reabsorption of urea. Essentially no
glucose is present in chicken urine and its reabsorption has been
studied (Pitts, 1938; Sperber, 1960; Dantzler, 1966). Data from

numerous sources indicate that sodium and/or potassium are

 

 

l3
reabsorbed in the chicken (e. g. Skadhauge and Schmidt-Nielsen
1967a; Sykes, 1971) but no detailed micropuncture studies have
been reported. An electrophysiological short circuit current
study indicates that, at least for the pigeon, the intensity of
active ion transport in the proximal and distal tubules is approx-
imately 50% and 25%, respectively, of that in the rat and this
transport is depressed similarly in the rat and pigeon by
furosimide and strOphanthin (Bessonov, 1972).

When the clearance of a solute exceeds the inulin
clearance (GFR) tubular secretion has occurred. Since uric acid
is the primary form of nitrogen excretion, its tubular secretion
has been extensively investigated (Sykes, 1971). It has been
shown that as much as 93% of excreted uric acid is contributed
by tubular secretion (Shannon, 1938). Rennick e_tal_. (1952),
using the Sperber (1948) technique and radioactive labelled
potassium, demonstrated that the potassium ion is secreted by
the chicken's kidney. Orloff and Davidson (1956, 1959) have
estimated the secretory transport maxima, and established com—
petitive inhibition with the hydrogen ion and non—competitive
inhibition with a mercurial diuretic. They suggest from these
data and others (Orloff and Burg, 1960) that all potassium
excreted is secreted in the distal tubule by a linked transfer of
potassium, hydrogen and sodium ions similar to that suggested

by Pitts (1958).

 

 

14

Renal response _tp osmotic challenge

 

 

Water loading was used by some of the early investi-
gators of renal function in the chicken to increase urine flow
(see David, 1927; Coulson and Hughes, 1930; Pitts, 1938). Pitts
(1938) suggested that GFR and urine flow were independent except
shortly after the bird had received a large dose Of water; then
both were elevated. After the administration of water a diuresis
curve with a concommitant decrease in urine osmolarity has been
Observed (Korr, 1939; Dicker and Halsam, 1966; Skadhauge and
Schrnidt-Nielsen, 1967a; Sykes, 1971). Dicker and Halsam (1966)
found two peaks in the diuresis. The first occurred within 20
minutes of water gavage which was thought to be neurogenic in
origin as a response to distension of the crop since it could be
reproduced by filling the crop with liquid paraffin. The second
coincided with the release Of water from the crop and absorption
by the gut. Korr (1939) attributed the increased urine flow to an
increase in the GFR from 1. l to 2. 5 ml per minute per kilogram
and not a decrease in water reabsorption; as he stated, ”on the
contrary more water is reabsorbed at high urine flow than at low
urine flow . . . . " Dicker and Halsam (1966) supported this
thesis; they did not measure GFR but instead used endogenous
creatinine excretion as an index of GFR. On the contrary
Skadhauge and Schmidt—Nielsen (1967a) found only a slight

increase in GFR and a large decrease in water reabsorption when

15
water loading a previously dehydrated rooster. The observed
change in urine flow rates was comparable to those measured by
Korr (1939). In all cases during the diuresis the urines became
very hypotonic. In chickens and turkeys a decrease in the
medullary-cortical osmotic gradient has been observed following
water loading (Skadhauge and Schmidt-Nielsen, 1967b). Sodium
excretion remains relatively unaffected during the diuresis
whereas potassium excretion is slightly enhanced and chloride

excretion is quadrupled (Sykes, 1971).

 

In the chicken, dehydration results in a decrease in
urine flow and an increase in urine tonicity (Korr, 1939;
Skadhauge and SchInidt-Nielsen, 1967a). Urine to plasma
osmotic ratios can become as high as 2. Urine is normally
isotonic or slightly hypotonic to plasma (Korr, 1939). Korr
suggested that GFR decreases during dehydration to approxi-
mately 50 percent of the control value. This was not substan—
tiated by Skadhauge and Schrnidt-Nielsen (1967a) who found only
a slight decrease in GFR as compared to water loaded birds.
These authors suggest that the rooster can resorb more filtered

water than mammals for a given urine to plasma osmotic ratio

_r"

because uric acid takes up little osmotic space as compared to

urea. They also found that more of the sodium chloride was

 

reabsorbed during dehydration than during water loading. The

medullary-cortical osmotic gradient during dehydration suggests

16
that a counter-current concentrating mechanism exists
(Skadhauge and Schmidt-Nielsen, 1967b).

When the chicken is given a salt load intravenously,
an initial diuresis occurs followed by a return to the initial value
or below depending on the intensity of the salt load (Korr, 1939;
Dantzler, 1966; Skadhauge and Schmidt-Nielsen, 1967a). Korr
(1939) found an increase and then a decrease in GFR paralleling
the change in urine flow whereas Dantzler (1966) reported only a
decreasing GFR was observed and Skadhaughe and Schmidt-
Nielsen (1967a) were unable to demonstrate any major changes in
GFR. Dantzler (1966) observed during continuous infusion of
hypertonic sodium chloride a rising urine and plasma osmolality
(urine osmolality was always less than plasma osmolality) and an
increase in the percent of filtered sodium excreted. Korr (1939)
was able to maintain a diuresis and GFR when infusing a hyper-
tonic solution at or above the urine flow rate, but Dantzler was
not. After infusion of 15 milliequivilents sodium per kilogram,
the rooster excreted a slightly hypertonic urine with a high rate
of excretion of sodium for the first hour followed by an increasing
rate of potassium excretion (Skadhauge and Schrnidt-Nielsen,
l967aL

A number of studies have been conducted on avian
species other than the chicken to examine their ability to COpe

with dehydration and/or salt loads (intravenous or drinking).

17
Primarily these investigations used birds adapted to either arid
or marine environments. The budgerygahs are small (30-40
grams) birds living in the arid interior of Australia. When given
0. 2 or 0. 3 molar saline they tend to stOp drinking and can sur-
vive without water for many days (some individuals as long as
130 days) with little loss in body weight (Cade and Dybas, 1962).
The apparent physiological response to dehydration is a slight
reduction in GFR (27%), an increase in filtered water reabsorbed
to greater than 99%, and an increase in filtered solute excreted
(Krag and Skadhauge, 1972). In water balance studies using
Gambel's, California, and Bobwhite quail which inhabit desert,
semidesert, and humid areas, reSpectively, differences in the
ability to cope with dehydration and salt loads were Observed
(McNabb, 1969a and b). The Gambel's quail has a lower mini-
mum requirement for water, higher tolerance for saline drinking
solutions, more stable plasma osmotic pressures, greater urine
to plasma osmotic pressure ratio and a larger prOportion of
medullary tissue in the kidney than the Bobwhite quail, with the
California quail generally intermediate. Carey and Morton (1971)
found that in addition to being able to process higher concentra—
tions of seawater and saline, and produce more concentrated
urine, the Garnbel's quail also adapts to arid conditions behav-
iorally (by reducing locomotor activity) during heat stress

further reducing water loss.

18

The savannah sparrows are able to withstand water
deprivation and drink seawater to varying degrees (Cade and
Bartholomew, 1959). The beldingi, a race of savannah sparrows,
is restricted to salt marshes and can produce urine with higher
urine to plasma ratios for osmotic pressure and chloride than
can the brooksi which breeds in fresh water marshes (Poulson
and Bartholomew, 1962). The beldingi can also tolerate higher
plasma osmotic pressures. Poulson (1965) attributes the ability
to produce a more concentrated urine to a greater proportion of
medullary tissue in the kidney, i. e. , more nephrons with IOOps
of Henle. This was essentially confirmed by Johnson and
Mugaas (1970a).

Many birds from marine environments, and some
from the desert, possess functional salt secreting glands, nasal
glands (Sturkie, 1965). The ducks and gulls have probably been
the most widely studied of these birds. The nasal gland is
necessary for the survival of ducks maintained on hypertonic
saline drinking water, i. e. , the kidney cannot handle the osmotic
load by itself (Bradley and Holmes, 1972). Following acute salt
loading with either hypertonic saline or seawater, there is a
diphasic, renal and extrarenal, response in gulls (Douglas, 1970)
and ducks (Holmes, e_t_al. , 1961). During the renal phase, there
is an increase in sodium excretion followed by a decline. In the

gull the sodium excretion can decrease below the initial rate.

19
The changes in sodium excretion are paralleled by changes in
urine flow rate and sodium concentration. The extrarenal phase
begins within one hour in the duck and 30 minutes in the gull. It
has been shown that a major prOportion of the excreted sodium
load leaves via the extrarenal route in gulls (Schmidt-Nielsen,
1960; Douglas, 1970; Hughes, 1970) and ducks (Holmes e_tfl. ,
1961; Holmes gal. , 1968). Hughes (1970) further suggests that
in the gull a major portion of the sodium and potassium was
excreted by the nasal gland in the absence of an osmotic stress.
It has been shown that the kidney is the primary pathway for K,
Mg, NH4, Ca and P04 excretion during osmotic stress (chronic
and acute) whereas for Na the kidney is the minor pathway
(Douglas, 1970; Holmes ital. , 1968).

The role 2: the adrenal

 

Corticosterone has been measured in the adrenal
venous and/or peripheral plasma of the chicken (Phillips and
Chester-Jones, 1957; Nagrae_tal. , 1960; Urist and Deutch, 1960;
Resko _e_t__a__l_. , 1964; Frankel ital. , 1967c; Taylor $911. , 1970),
the turkey (Brown, 1961; Nagra S‘ifl' , 1960), the pheasant
(Nagra gta_l. , 1960), the duck (Boissin ital. , 1966; Boissin,
1967; Macchi e_ta_l. , 1967; Donaldson and Holmes, 1965; Bayle
_e_tal. , 1971), the quail (Bayle 23:11. , 1971), the pigeon (Bayle

£231. , 1971), and the gull (Macchi _e_tgi. , 1967). The relative

merits of the techniques used has been discussed in two recent

20
reviews (Frankel, 1970; Sandor, 1972). Frankel £11. (1967c)
and Taylor e_ta_1. (1970) have determined the concentration of
corticosterone in adrenal venous plasma to be 7. 3 and 8. 0 mg/
100 ml, respectively, in the chicken. In the duck the secretion
rate for corticosterone is 2. 43,.g/minute/kg (Donaldson and
Holmes, 1965).

Phillips and Chester-Jones (1957) were the first to
measure aldosterone in the adrenal effluent blood of chickens.
Subsequently, Taylor _eial. (1970) and Sandor (1972) using the
sensitive double isotOpe derivative assay have determined the
concentrations to be 0. 21 (adrenal venous) and 0. 014 (peripheral)
mg/100 ml plasma in the chicken and duck, respectively.

DeRoos (1960, 1961), and deRoos and deRoos (1963)
were the initial investigators of gay—ital corticosterone and
aldosterone synthesis by the avian adrenal. Donaldson e_ta_1.
(1965) established that 18-hydroxy-corticosterone is also an
adrenal secretory product 23:21:12. Numerous other investi-
gators have used HEELS). preparations of avian adrenal to study
steroidogenesis and/or steroidsecretion (see Frankel, 1970;
Sandor, 1972). Steroidogenic pathways in the avian adrenal are
only partially understood. Sandor (1972), based on the work of
many investigators, has prOposed a schema (Figure 1) for the
biosythesis of adrenal steroids. One should bear in mind that

this is a composite schema using data from different avian

21

Acetyl-COA

Cholesterol

Pregnenolone— -- — - -- - - -— .1

Cortisole— -— -— — — —- Progeseterone—_——.)1 l-hydroxy-
progesterone

 

19-hydroxy-

11-deoxy- ¢
corticosteroneE—l1-deoxycorticosterone ‘- _ ._ ._ _ .—

 
    

........A.L.....................

 

’ ’ ’
z
’ ’
11-dehydro- ’ ’ lB-hydroxy-
corticosteroneQ— 4Corticosteron£ ——sycorticosterone|

 

, (20 18 cyclicl
/ hemikotal)
’ I
I

/ l
Aldosterone‘n — -— .. -— .— — _o ._. .

Figure 1

Biochemical pathways of steroidogenesis
in the class Aves

Note: The solid lines represent validated pathways whereas the
' broken lines are postulated pathways.

22
species and gathered 13mg. £11321? validation is still forth-
coming.

Many researchers have adrenalectomized avian
species including the chicken, the duck, and the pigeon (see
Sturkie, 1965). Herrick and Torstyeit (1938) reported that
chickens could be maintained as long as 82 days after a few
injections of cortical extracts with continuous 1. 6% saline
drinking water and normal saline administered intramuscularly.
Others have not been successful with NaCl in the drinking water
(Taber _etil. , 1956). Deoxycorticosterone acetate (DCA),
cortisone, cortisol and cortical extracts have been used to main-
tain avian species after adrenalectomy (Bulbring, 1940; Miller
and Riddle, 1943; Brown _e_til. , 1958b; Phillips e_ta_1. , 1961).
There has been little concern with electrolyte excretion follow-
ing adrenalectomy. Brown e_ta_1. (1958b) made the surprising
observation that following adrenalectomy sodium excretion
decreased, potassium excretion showed no change in the chicken
and urine volume remained normal. Serum sodium was slightly
depressed whereas potassium was significantly increased. DCA
(4 mg/kg/day) did not, whereas cortisone (10 mg/kg/day) did,
restore sodium excretion. Serum sodium and potassium concen-
trations were restored by DCA and cortisone treatment. In the
duck, adrenalectomy appeared to increase sodium and water

excretion after saline loading (Phillips e311. , 1961). When

23
cortisol (5mg/day) was administered, these changes were
corrected.

Holmes and his collaborators have studied the
effects of exogenous adrenocortical hormones on total renal
excretion of sodium and potassium in the saline-loaded and
water-loaded duck, a bird with a functional nasal gland. The
ducks were treated with 5 mg (im) of cortisol and deoxycorti-
costerone at 12 and 1. 5 hours and 250pg (im) of aldosterone at
1. 5 and 0 hours prior to saline loading (Holmes _e_til: , 1961).
Cortisol decreased sodium excretion but did not affect potassium
excretion or urine volume during the osmotic diuresis. Deoxy-
corticosterone had no significant overall effects on the diuresis
whereas aldosterone produced striking negative effects on urine
volume, sodium output, and potassium output. In another
experiment, the ducks were given 25 milliliters of distilled
water at 0, 1. 5, 3. 0, and 4. 5 hours and injected intramuscularly
with corticosterone (1. 25 or 2. 50 mg), cortisol (l. 25 or 2. 50
mg), or aldosterone (50 or 100pg) at -l. 5, 0, 1. 5, 3. 0 and 4. 5
hours (Holmes and Adams, 1963). Increases in urine volume
and potassium excretion accompanied by a decline in sodium
excretion were observed in birds treated with cortisol and corti-
costerone. Aldosterone caused highly significant retention of
sodium and potassium with no effect on urine volume. In the

chicken, Brown e_ta_1. (1958a) increased daily urine volume using

 

 

24
the unnatural steroids DCA and cortisone but Observed con—
trasting results on sodium and potassium excretion. A decline
in daily renal sodium (significant) and potassium (borderline)
output was observed in birds treated with DCA (4mg/kg /day) but
cortisone (15mg/kg/day) increased both significantly. Orloff and
Burg (1960) briefly state that aldosterone, 2-methy1-92-fluoro-
hydrocortisone, and desoxycorticosterone did not affect electro-
lyte excretion when administered into the portal system though

no data, dosages, or procedures were presented. No change in

 

the adrenal venous concentration of corticosterone or aldo-
sterone was Observed after sodium depletion of the chicken
(Taylor et a1. , 1970). A size increase in the peripheral zone of
the adrenal was reported by these authors. The biological half-
lives and apparent volumes of distribution of exogenous corti-
costerone and aldosterone were 8. 25 minutes and 780 ml/kg for
corticosterone, and 8. 34 minutes and 6400 ml/kg for aldo-
sterone; these were unaffected by low or high dietary sodium
intake in the duck (Thomas and Phillips, 1972).

The regulation of avian adrenal cortical function
through the hypothalamus and adenohypophysis is similar to that
in mammals with one notable exception (see Frankel, 1970, and
Wells and Wight, 1971 for reviews). After adenohypophysectomy

the concentration of corticosterone in the plasma is reduced but

 

not to the extent which it is suppressed in mammals. Lines of

25

evidence have been advanced that indicate there is an extra-
hypophyseal source of corticotrOphin-like activity and this
source is in the hypothalamus (e. g. , Frankel e_tfl. , 1967b;
Salem e_ta_1. , 1970a, b; Bayle _e_tal. , 1971; Bouille and Bayle,
1973). Bradley and Holmes (1971) found no need to suggest the
presence of this extrahypophysial source in the adenohypOphy-
sectomized duck.

In contrast to corticosterone very little is known

about the regulation of aldosterone secretion by the avian adren-

 

al. EM, deRoos and deRoos (1963) were able to stimulate
aldosterone production with AC TH but not angiotensin 11. Early
work by Phillips and Chester—Jones (1957) indicated that ACTH
increased aldosterone in the adrenal effluent blood (_i_r_1V_iv_q), but
this was not substantiated by Taylor $2.1: (1970) using a more
sensitive and specific assay. Following hypophysectomy the
biological half-life is prolonged and the metabolic clearance rate
diminished for aldosterone in the duck (Bradley and Holmes,
1971) and pigeon (Chan 2.5.3.21: , 1972). Bayle e_ta_1. (1971)
observed no change in the adrenal content of aldosterone in the
hypOphysectomized quail, duck, and pigeon. In the chicken,
hypOphysectomy and ACTH have no effect on aldosterone in the K
adrenal effluent plasma (Taylor e_ta_1. , 1970).

Many investigators have demonstrated the presence

 

of a renin-angiotensin system in Aves (Bean, 1942; Schaffenburg

26
_e_tgi. , 1960; Capelli e_ta_1. , 1970; Chan and Hohnes, 1971; Nolly
and Fasciolo, 1972, 1973). Hemorrhage increased plasma renin
activity (Chan and Holmes, 1971). Following hypophysectomy,
these authors observed an increase in plasma renin activity but
renin plasma substrate decreased. Sodium depletion was asso-
ciated with an increased granulation of the juxtaglomerular cells
and increased renin content of the kidney but no change in
adrenal plasma aldosterone content (Taylor _e_tfg. , 1970).

The role 91 the neurohypOphysis

 

NeurohypOphysectomy produces polydipsia and
polyuria in the chicken (Shirley and Nalbandov, 1956), and the
duck (Wright e_ta_1. , 1967; Bradley e_ta_1. , 1971). Bradley e_ta_1.
(1971) also Observed increased sodium, chloride, and total
osmotic activity excretion rates but no change in potassium
excretion rates. Hypothalamic lesions produced similar results
accompanied by a decrease in neurohypophysial pressor
activity (Koike and Lepkovsky, 1967). The neurohyp0physia1
hormones in aves are vasotocin (8-arginine oxytocin) and oxyto-
cin (Munsick e_ta_1. , 1960; Munsick, 1964), and/or vasotocin and
mesotocin (Archer, 1971). In the hydrated chicken, vasotocin
produced an antidiuretic effect (Munsick fetal. , 1960). Bradley
_e_tal. (1971) were able to reverse the effects of neurohypophy-
sectomy (see above) with vasotocin but arginine vaSOpres sin only

returned the urine flow to normal. Skadhauge (1964) has shown

 

 

27
that vasotocin exerts its antidiuretic effect on the renal tubule
(GFR and renal plasma flow were unaffected) from the serosal
side. Blood levels of vasotocin have been reported in the chicken
(Douglas and Sturkie, 1964; Sturkie and Lin, 1966) and in the
chicken, quail, and pigeon (Niezgoda and Rzasa, 1971).
Niezgoda and Rzasa observed higher blood levels of vasotocin in
the males (all species); they suggested this might account for the
higher water intake by hens observed by Lifschitz e_ta_1. (1967).

An increase in vasotocin during oviposition has been reported

 

(Sturkie and Lin, 1966); Sykes (1971) observed a delay in the
diuresis due to water loading at this time. Though there are no
reports on vasotocin in the circulation following the apprOpriate
osmotic stimuli, there are reports on its depletion from the
neurohyp0physis following dehydration and salt loading (e. g.
Lawzewitsch and Sarrat, 1970; Follet and Farner, 1966).

Other considerations

 

The work by Ensor and his collaborators indicate that
prolactin is involved in the mineral and water metabolism of the
duck (Ensor and Phillips, 1970, 1972; Ensor e_tal. , 1973). They
have established that it acts as an antidiuretic and is involved in
nasal gland functions.

McNabb e_ta_1. (1973) have demonstrated that sodium
and potassium are excreted in the urate precipate fraction of the

chicken's urine in significant quantities. This may aid in their

 

28
excretion by reducing their contribution to osmotic pressure.
The role of peritubular oncotic pressure has been investigated in
the chicken using the Sperber technique (Vereerstraeten and
Toussaint, 1965, 1968). They concluded that the oncotic pres-
sure has an antinaturetic effect and therefore plays a role in
sodium transport by the renal tubules.

The Cloaca, Colon, and Ceca

 

Investigators as early as Winer (1902) suggested that

water may be reabsorbed by the colon. Korr (1939) presented

 

data indicating that post renal isosmotic reabsorption could occur.
It was observed that birds with exteriorized ureters and
colostomies required 1% sodium chloride in the diet and showed

a greater rate of weight loss during dehydration than intact

birds but water consumption was not greater (Hart and Essex,
1942); Dixon (1958) did not observe high water intake or excre—
tion in chickens with exteriorized ureters or colostomies. In
contrast to these observations, Dicker and Halsam (1966)
recorded a 64% increase in water intake after exteriorization Of
the ureteral openings. In another experiment, those authors .

observed a smaller increase (25%) which could be attributed to

 

urine loss (Dicker and Halsam, 1972). Numerous researchers (
have shown that urine moves retrogradedly from the cloaca into
the colon and ceca (Koike and McFarland, 1966; Akester eta—l. ,

1967; Nechay e_ta_1. , 1968; Skadhauge, 1968; Ohmart e_ta_1. ,

29
1970). Recent evidence suggests that during dehydrations post-
renal reabsorption may play a significant role in water and
electrolyte balance (Skadhauge, 1967, 1968; Bindslev and
Skadhauge, 1971 a, b). The technique used by Skadhauge may
prove to be fruitful in the investigation of the physiological
importance of post-renal urine modification. Arginine vasotocin
had no effect on reabsorption of water and sodium in the colon of
the chicken (Skadhauge, 1967). The influence of other hormones,

notably the cortical steroids, on post-renal urine formation has

 

not be en inve stigated.

 

MATERIALS AND ME THODS

Experiment 1

 

This experiment was designed to Observe the effects
of corticosterone and aldosterone during the first ninety-five
minutes when aldosterone and corticosterone were being infused

intravenously at near estimated secretion rates. These rates

 

were based on the work of Donaldson and Holmes (1965) in the
duck on corticosterone secretion (2. 43 pg/min/kg) and the ratio
of corticosterone to aldosterone (40:1) in adrenal venous blood of
the chicken (Taylor e_ta_1. , 1970).

The experimental animals used in this study were
mature Single Comb White Leghorn (SCWL) roosters. These
animals were from the stocks maintained on the Poultry Science
Research and Teaching Center at Michigan State University.
They ranged in weight from 1. 6 to 2. 7 kilograms (kg). Prior to
experimentation the roosters were transferred from the Center
to an environmentally controlled room with 17 hours daily of

light commencing at 6 A. M. and a temperature of 210C, and were K

 

housed in individual wire cages. Feed and water were supplied
fl libitum.

30

31

Prior to surgery for separating the ureters from the
alimentary tract, the roosters were removed from their cages
between 7:30 and 9:00 A. M. at which time they were anesthetized
with 150-160 mg/kg body weight of sodium phenobarbital. No
sustaining anesthesia was needed. The femoral vein was
isolated through an incision in the lateral surface of the lower
thigh and the m. iliotibialis. An in-dwelling cannula of poly—
ethylene tubing (Intramedic PE 190) was inserted proximally in

the incised vein approximately 4 to 5 centimeters (cm). This

 

cannula which was filled with heparinized saline (40 units/ml)
was used to collect blood samples throughout the duration of the
experiment.

The rooster was restrained in the upright position on
a V-shaped bird board. The tail was extended cranially and the
feathers removed from the cloacal and abdominal regions. The

dorsal lip of the cloaca was lifted dorsally to its limit and

 

fastened in place with a midline stitch and two stitches were
made 4—5 millimeters (mm) to either side of the midline incision.
The cloaca was temporarily held Open with two pair of Allis
intestinal tissue forceps (6 inch) attached laterally to the lip of
the cloaca. A suture was passed through the dorsal portion of
the uro-proctodeal fold in the midline. This suture was used to
fasten this fold dorsally, thus exposing the uretral Openings.

With this technique the uretral openings are partially turned

 

32
toward the midsaggital plane and the urine flows into a midline
trough formed by stretching the uro-proctodeal fold dorsally.
Any fecal matter in the coprodeum was then removed. The
coprodeum was filled with cotton and closed by cross-stitching
the coprourodeal fold. In order to continuously wash urine from
the uretral openings a section of polyethylene tubing (Intramedic
PE 190) was fastened in the midline dorsal to the uretral openings.
Water running from this tube would flow ventrally through the

trough formed from the urodeal-proctodeal fold. The urine was

 

washed into tared centrifuge tube with deionized distilled water
delivered by Harvard Infusion/Withdrawal pump (Model 940,
Harvard Apparatus Co. , Inc. , Millis, Mass.) at a rate of

0. 39828 grams per minute. Starting at the ventral midline the
cloacal lip was sutured over a Teflon funnel 3 cm x 4 cm, I. D.
x O. D. The sutures were placed at 5 mm. intervals alternately
to the left and right until slightly over 180 degrees of the circle

was fastened to the cloacal lip. Using this procedure each

 

rooster was prepared for urine collection.

The right brachial vein was isolated in the humoral
region and cannulated proximally with polyethylene tubing (Intra-
medic PE 60) for the infusion of 14tC-inulin (see below). The
cannula was attached to a 3-way non-pyrogenic plastic stOp-cock
and filled with heparinized saline (40 units/ml) and inserted

proximally into the incised vein approximately 6 cm. If blood

 

33

could be withdrawn easily, the cannula was considered to be in
the vena cava; if not, it was inserted a few more millimeters
until blood could be withdrawn easily. In a similar manner the
left brachial vein was cannulated for infusion of the adrenal
cortical hormones (see below).

Urine was collected for ten minute periods in tared
polyethylene centrifuge tubes (15 x 120 mm). Immediately after
collection, the centrifuge tube was sealed with Parafilm and

stored at room temperature until the end of the experiment. At

 

this time, the tubes containing the urine were weighed on a
Mettler analytical balance to the nearest 0. l milligram (T2 in
formulas below). These tubes were centrifuged at 1500 rpm for
ten minutes in an International Centrifuge (Model SBV) to
separate the precipitated urates from the liquid phase of the
urine. The supernatant was decanted into a 1 dram screw cap

vial made of borosilicate glass and capped. The centrifuge tube

containing the precipitate (T3 in formulas below) was allowed to

 

drain dry on a paper towel for 24 hours before being weighed
again. Using the following formulas it was possible to determine
the volume of the urine (assuming 1 gram : 1 milliliter), and
the dilution factor for the urine:

V(m1/min): [(TZ - T3) - 3. 9828] / 10 min.

Dilution Factor 2 (T2 — T3)/[(T2 - T3) - 3. 9828]

For subsequent determination of glomerular filtration rate

 

34
(GFR), O. 2 ml of the supernatant was set aside. The remainder
was stored in a freezer at .-18. 5°C until sodium (Na+) and
potassium (K+) analyses could be conducted.

Inulin clearance (Co = GFR) was determined using

in

14C-inulin (Arnersham/Searle Corporation). A stock solution of

14 . . . . . .

C-1nu11n was made to contain two microcurles (1‘ C1) per ml.
in 0. 9% saline with l. 0% of benzyl alcohol. Each subject was
given a priming dose consisting of 0. 9 ”Ci/Kg body weight‘of

4C-inulin from the stock solution through the cannula in the right

 

brachial vein. Through the same cannula a l4C-inulin infusion of
approximately 0. 007 pCi/min/Kg was maintained until the end of
the experiment at 0. 16 ml/min using a Harvard Compact Infusion
Pump (Model 975). A minimum of 60 minutes was allowed before
inulin clearances were measured. At the midpoint of the ten
minute clearance period 2. 5 ml of blood were removed and
heparinized through the cannula in the right femoral vein and 2. 0

m1 of 0. 9% NaCl solution were replaced through the same

 

cannula. The blood was placed in a tapered polyethylene centri-
fuge tube and centrifuged at 1500 rpm for ten minutes in an
International Centrifuge (Model SBV). This was transferred to a
one dram screw cap vial; 0. 2 ml of plasma were pipetted into a
scintillation vial containing 10 m1 of Bray's solution (Table 1)
and the remainder was stored with the urine (see above) until

Na+ and K+ analyses could be conducted. A Model 724 or 6848

 

35
Nuclear Chicago (Nuclear Chicago Corp. , Des Plaines, Ill. )
liquid scintillation counter was used to count the plasma and
urine samples for ten minutes. Sample counts were corrected
for background. No quenching was observed with either plasma

or urine. GFR was calculated as follows:

 

U V
GFR = C = In
In PIn
Where,
V = volume of urine (ml/min)

 

 

 

UIn = urine concentration of inulin

([CPM/. 2 ml - Background] x dilution factor)
Pln = plasma concentration of inulin

(CPM/. 2 ml - Background)

TABLE 1

Composition of Bray's Solution
Chemical Amount
Naphthalene 60 grams
PPO 4 grams '
POPOP 200 milligrams
Methanol 100 milliliters
Ethylene glycol 20 milliliters
p-dioxane to 1 liter K

 

 

Source: Bray, 1960

36

The concentration of Na+ and KJr in the plasma and
urine samples were determined with a Jarrel Ash (Model 2)
Atomic Absorption Spectrophotometer using the emission mode.
This unit was attached to a strip-chart recorder through a
custom built signal modifying box, so that the signal could be
recorded. Na+ and K+ determinations were made at approxi-
mately 5889 A and 7655 A, respectively, with fine adjustments,
for maximum peak height, made prior to each run. The plasma
and urine samples were thawed and brought to room temperature.
Plasma samples were diluted 1:100 and 1:10 with deionized dis-
tilled water for Na+ and K+ determinations, respectively. Urine
samples were diluted with deionized distilled water 1:5, 1:8,
1:10, or 1:16 (1:8 used normally). Standard solutions of NaJr
(0.2, 0.8, 1.4, and 2.0 meq/l) and K+ (0.12, 0.48, and 1. 20
meq/l) were used for determining a standard curve for each run.
These standards were found to fit a simple linear regression
line (Steele and Torrie, 1960) of the following form:

log [peak height (mm)] : b0 + b1 [concentration of

NaJr or K+ (meq/l)]

The concentration of the unknown samples was
determined from the prediction equation.

Plasma Na+, plasma K+, urine Na+ and urine KJr
concentration was obtained by correcting the unknown samples

for dilution factor(s).

 

 

37

The adrenal cortical hormones used in this study
were aldosterone (4-pregnen-18-al-11B, 21-diol-3, 20-dione),
and corticosterone (4-pregnen-11B, 21-diol-3, 20-dione). They
were obtained in pure form from Schwartz/Mann Chemical
Corporation. Solutions of 5. 0 mg/ml and 0. 1 mg/ml in 95%
ethanol were prepared from corticosterone and aldosterone,
respectively. These solutions were further diluted with 95%
ethanol so that when infused into the left brachial vein at a flow
rate of 0. 02 ml/min with a Harvard infusion/withdrawal pump
(Model 950) they would be delivered at 0. 04, 0. 08, 0.12 and 0.16
pg/min for aldosterone, and 3. 0, 6. 0, 9. 0 and 12. 0 p g/min for
corticosterone.

Ninety minutes after surgical preparation and inulin
priming, each rooster was infused with either aldosterone,
corticosterone, or 95% ethanol (control) for 95 minutes. During
this time, urine was collected for nine ten minute clearance
periods with no urine collection between 50 and 55 minutes so
that urine wash and 14C-inulin syringes could be refilled. Four
or five roosters were used for the test substances at each level.
Measured and derived parameters for the clearance periods are

shown in Table 2.

 

 

38
TABLE 2

Parameters Measured in Experiments 1 and 2

 

 

Parameter Symbol Experiment
Glomerular filtration rate GFR 2 cm 1, 2
Urine flow rate (fluid) V l, 2
Plasma concentration of X PX l

Urine (liquid phase)
concentration of X UX l, 2

Urine (liquid phas e)

excretion rate of X EX 1, 2
Filtered load of X FX 1
Clearance of X CX 1
Percent FX excreted %EX 1
Percent water reabsorbed Reab H20 1, 2
Change in body weight ABW 2
Solid urine (urates) Ur 2

 

Urine (solid phase)
excretion rate of X --- 2

Urine (total) excretion
rate of X --- 2

Percent of X excreted
in solid urine --- 2

 

 

39

Experiment _2_

 

This experiment was designed to test the effects of
corticosterone and aldosterone on the renal function of the adult
male chicken when administered intramuscularly at four times
the estimated secretory rate (see Experiment 1) for three days.
Since birds excrete part of their urine in solid form (urates), the
comparison of the sodium and potassium excretion in the liquid
portion of urine was to be made with that in the total urine (liquid
and solid) to aid in the interpretation of the results from Experi-
ment 1 (in which only liquid urine was measured).

The roosters used in this experiment were selected
from the stocks maintained on the Poultry Science Research and
Teaching Center. They were Single Comb White Leghorn of the
Ghostley strain and were between 12 and 18 months of age. Prior
to use they were brought to the cage room in Anthony Hall,
weighed and maintained on a layer ration in wire floored bat-
teries until the experiment was terminated. The light regime in
the Anthony Hall location was 14. 5 hours of light daily com-
mencing at 6:30 A. M.

The protocol for this experiment called for ten birds
to be divided into three experimental groups. Two groups con-
tained three birds each; one of these was treated with . 35 mg/kg/
day of d—aldosterone (CIBA Pharmaceutical Corp. ; Summit,

N. J.) and the other with 14. 0 mg/kg/day of corticosterone

 

 

40
(National Biochemical Corp. ). The aldosterone was carried in
safflower oil (. 35 mg/ml) and administered intramuscularly four
times daily at equal intervals alternating between the right and
left thighs, starting at 8:00 A.M. of day l and ending at 8:00 A. M.
of day 4 (72 hours later). The corticosterone was administered
as a stabilized suSpension (10 mg/ml) in 0. 9 percent saline with
1 percent methylcellulose and following the same schedule as the
aldosterone group.

The third group contained four birds and acted as the
control group. One half of these birds were treated with the
aldosterone carrier and the others with the corticosterone carrier
on the schedule described previously. Treatments were
assigned randomly to days since only one bird could be pre-
pared for urine collection per day. The birds were weighed at
8:00 A. M. of day l and day 4. Feed was removed after the
lights went off on the last day of treatment to aid in the surgical
preparation for urine collection.

Between 10:00 and 11:00 A. M. of day 4, the birds
were anesthetized with sodium phenobarbital (120—160 mg /kg)
and received 3-4I‘Ci/kg of 1‘JIC-inulin (2 ”Ci/ml) in 9. 0 percent
saline. They were prepared for urine collection as described in
Experiment 1. Approximately 90 minutes following anesthetiza-
tion, a 30 minute urine collection was made. The urine was

washed from the funnel with deionized distilled water delivered

 

41

by a Harvard infusion pump at the rate of 10. 8186 gm/30 minutes
into a tared, to the nearest 0. 1 mg, borosilicate glass test tube
(18 x 150 mm). Care was taken to make sure no solid urine was
adhered to the funnel at the end of the 30 minute period. Blood
was withdrawn from the vena cava through a polyethylene cannula
(Intramedic PE 50; Clay Adams Corp. ), inserted via the left
brachial vein. One milliliter was collected at 5, 15, and 25
minutes, in a heparinized 2. 5 ml plastic syringe, after the start

of urine collection. The blood was replaced with 0. 9% saline.

 

The collected urine, after weighing, was cooled over-
night at 50C and centrifuged at 2500 rpm in an International Cen-
trifuge (Model SBV) for 20 minutes. The liquid portion of the
diluted urine was decanted into a borosilcate test tube, sealed
and stored at 40C until the sodium, potassium and inulin analy-
ses were performed. The solid portion Of the urine (urates) was
dried overnight in an oven at 700C and then stored in a one dram
screw cap vial until sodium and potassium analyses were per-

formed. The blood samples were centrifuged at 1500 rpm for 10

 

minutes in the same centrifuge. The plasma was stored in a one
dram screw cap vial at 40C until inulin analysis was performed.
The inulin concentration expressed as cpm per milli-
liter was determined liquid scintillation counting in Bray's
solution as described in Experiment 1 using 0. 1 ml samples of

plasma and diluted urine. The urine concentration was corrected

42
for the dilution.

Sodium and potassium concentrations in liquid and
solid urine were analyzed by flame emission spectrophotometry
using a 11 453 Atomic Absorption Spectrophotometer (Instrument
Laboratory Corp. ). The analyses of the liquid urine were per-
formed basically the same as in Experiment 1 except that the
dilutions were approximately 100 fold greater due to the increased
sensitivity of this spectrOphotometer. In order to solubilize the
urates, approximately 10 mg of solid urine were placed in a
borosilicate glass test tube and 0. 5 ml of analytical grade con-
centrated sulfuric acid was added. After the urates dissolved,
9. 5 ml Of deionized distilled water were added. This caused the
uric acid to precipitate and is a modification of the procedure
described by Porter (1963a) for the preparation of spectro-
scopically pure uric acid. These were then centrifuged at 2500
rpm for 20 minutes in the International Centrifuge (Model SBV)
and diluted with deionized distilled water to fall into the range of
the standards. The standards used were 8 to 20 x 10-3 meq/l
for sodium and 4 to 14 x 10"3 meq/l for potassium. The final
concentrations were expressed as meq/l for liquid urine and
meq/mg for solid urine.

Statistical Analyse s

 

The statistical design of the first experiment was a

two-factor split-plot factorial design (Kirk, 1968). The

 

 

43

independent variables (parameters) were subjected to analysis of
variance (ANOVA) to determine primarily if there was an inter-
action between level of hormone and time after infusion or an
experiment-wide time effect. When an interaction existed,
further ANOVA was used to determine which treatment levels
varied significantly over time since a time trend was expected.
Within those treatments which showed significant time effects a
”t" test was used for mean separation. Separate analyses were
conducted for the aldosterone and corticosterone data with the
same set of birds acting as controls (zero level of hormone).

The second experiment was a one-factor completely
randomized design (Kirk, 1968). The data were subjected to
ANOVA and when significant effects were found Duncan's New

Multiple Range test was used for mean separation.

 

RESULTS AND DISC USSION

Plasma Sodium and Potassium

 

Plasma sodium concentrations (PNa) remained stable
throughout the duration of the experiments (Figures 2 and 3).
There was a wide range of PNa between groups in the aldosterone
(. 08 [Ag/min mean = 135. 6 meq/l and . 12pg/min mean = 165. 6
meq/l) and corticosterone treatments (9. 0fig/min mean = 141. 4
meq/l and 12. Opg/min mean = 166. 2 meq/l). This did not appear
to be related to treatments but to variations among individuals.
The variation within individuals over time was small. Because

of this stability, an average P a for each individual was used in

N
calculating filtered load of sodium (FNa) and percent of filtered

load excreted (%E ). Some reported mean values range from

Na
132 to 180 meq/l in domestic chickens (Dantzler, 1966; Kravis
and Kare, 1960; Skadhauge and Schmidt-Nielsen, 1967a; and
Vereerstraeten and Toussaint, 1968).

Plasma potassium concentrations (PK) were not as
stable as PNa during the experiments (Figures 4 and 5). Though
there were variations between treatment groups these did not
appear to be dose dependent. The PK observed in these
44

45

«kcontrol
O 3. 0 pg/min corticosterone
Cl 6. 0 ug/min
180 {K 9. OPg/min
O 12. 0 lag/min

170
./ .x._—-—.-——.~.—-—.
."‘""
/\
160 /0
PN a
(meq /1)

150

140

130

     

1 5 30 45 60 75 90

minutes

Figure 2

Plasma sodium concentrations during
the 95 minutes of corticosterone
infusion

 

180+

 

46

4k control means

 

O . 04 hg/min aldosterone
D . 08 pig/min
¢K . 12pg/min
* O . 16 gag/min
1704 \
/ fi’*W*—*\fi’fi
/ *
PNa \*——'* \ /
(meq/l) . *
C
1504 \ /
\/ O O \.
o-""O\ / O/
1404
[I‘D—D
C] /D\a/ \D
1304
V V V V
3'0 45 60 75 90
minutes
Figure 3

Plasma sodium concentrations during the
' '95 minutes of aldosterone infusion

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49
experiments are compatible with those previously reported in
domestic chickens (see Kravis and Kare, 1960; Orloff and
Davidson, 1959; and Skadhauge and Schmidt-Nielsen, 1967a). In
the aldosterone, corticosterone and controlgroups individuals
exhibited fluctuating PK with time. These fluctuations varied
among individuals but, when all treatment groups were averaged
together, PK increased during the first 25 minutes then declined
to a low at 45 minutes followed by a steady increase until the
experiments were terminated (Figure 6). Analysis of variance
of the means, using time as a treatment, detected no differences
(p) . 10). Due to these variations, the PK measured at each
time period was used in calculating FK and %EK.

Glomerular Filtration Rate (GFR)

 

The GFR's measured in Experiments 1 and 2 are
displayed in Tables 6, 7, and 8. In Experiment 1 there was con-
siderable variation between and within individuals. Observed
GFR's ranged from . 62 to 4.12 ml/min/kg though most were
between 1. 0 and 3. 0 ml/min/kg as has been reported by others
(Pitts, 1938; Korr, 1939; Sperber, 1960; Dantzler, 1966;

Langford and Fallis, 1966; Skadhauge, 1964; Skadhauge and
Schmidt-Nielsen, 1967a). The variability within birds was often
twofold and occasionally threefold. Similar findings have been
reported by Langford and Fallis (1966). Both the previous authors

and myself used general anesthetics whereas Skadhauge and

50

H “doaflnomxm an mnoumoou
2m mo mcoflmuucooaoo gammduom «893% “302

o onswfih

mouficfie

cm on on cm on 0v on o N

 

G608

Hm

or

51
Schmidt-Nielsen (1967a), who did not report variations of this
magnitude, used only local anesthetics. It is possible that the
general anesthetics (barbiturates) might interfere with neural
control of glomerular filtration. In Experiment 2, the range of
GFRs was considerable less (1. 51 to 2. 60 ml/min/kg). This
may have been the result of longer collection periods (30 vs. 10
minutes), less observations, and/or more homogeneity between
birds.

In Table 6 can be seen the effect of corticosterone
infusion 0n GFR. ANOVA indicated there was a significant
(p < . 05) treatment by time interaction as well as treatment and
time effects (Table 3). Corticosterone at 6. 0 and 9. 0 fag/min
caused significant increases in GFR by 55-75 minutes which then
declined during the 75-95 minute period. This showed some dose
dependency (Figure 7), but (paradoxically) at the highest level
GFR was unaffected (Table 6).

Glucocorticoids have been shown to increase GFR in
the adrenalectomized dog (Garrod e_tal. , 1948) but not in normal
men (Dingman e_ta_1. , 1958). The changes seen in this experi-
ment appeared to be transient as they were declining by the end
of the experiment. This was further supported by the second
experiment (Table 8) in which, after three days of corticosterone
treatment, no significant change in GFR was observed.

Aldosterone had no effect on GFR in the acute

mo.V m V“.

 

 

 

52

 

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m HAfl/WH.

 

53

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GFR .60
(ml/min/kg)

.40

.20

 

 

 

 

       

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Figure7

The effect of corticosterone infusion rates
on mean changes in glomerular filtration
rate at 55-75 minutes from 0-30 minutes

54
(Table 7) or chronic (Table 8) experiments. Others have
Observed that aldosterone does not affect changes in GFR when
administered to dogs (Garrod _e_t__ail_. , 1955) or man (Yunis 9.5.31: ,
1964; August e_ta_1. , 1958). It is important to note that there was
no overall effect of time in the acute experiment indicating that
no significant dehydration occurred due to urinary or evaporative
water loss. Korr (1939) and Skadhauge and Schrnidt-Nielsen
(1967a) reported reductions in GFR during dehydration;
budgerygahs also showed a slight reduction in GFR during dehy-
dration (Krag and Skadhauge, 1972).

Tubular Function

 

Urine flow and water reabsorption

 

The rate of urine formation showed a significant
increase when corticosterone was infused at 9. 0 and 12. 0 p g/min
(Tables 3 and 9). The change had a greater magnitude and
occurred earlier (30-50 vs 55-75 minutes) when the higher dose
was given. There was an inverse relationship between percent
water reabsorbed (Reab H20) and urine flow (Figure 8) and the
12. 0 pg/min treatment produced a significant depression in
Reab H20 by 30-50 minutes (Table 10). The increase in urine
flow in the 9. 0flg/min group was not accompanied by any signi-

ficant depression in Reab 20 (Table 10 and Figure 8) but this

H

group had the highest average GFRs and a significant increase in

GFR due to corticosterone administration. This suggests that

 

Reab H20 ((70)

55

100
«99
99 0 t9
0 (9
§ O
on: 8 0 9. OPg/min corticosterone
*
98 O 0 control + all other
. . corticosterone treated
. birds

 

20 40 60 80 100
V("1/min/kg)
Figure 8

Relationship between urine flow rate and
water resorption in control and cortico-
Sterone treated roosters in Experiment 1

56
the diuresis observed was due primarily to the increased filtra-
tion rate. In contrast, the diuresis observed at the higher dose
appeared to be the result of a depression in water resorption.
When 14 mg/kg/day corticosterone (Experiment 2) was adminis-
tered i.m. for three days, a significant diuresis was produced
which was due to decreased water resorption (Table 5, 8 and
Figure 9).

When aldosterone was infused for 95 minutes or
injected intramuscularly for three days there were no effects on
urine flow or Reab H20 (Tables 8, 11, 12). In the acute experi-
ment (1) there was a significant time effect on both urine flow
and Reab H20 (Table 4). The rate of urine excretion began to
increase at 55-75 minutes; this was accompanied by corres-
ponding decreases in Reab HzO (Tables 11 and 12). This may
reflect a depression in the secretion of arginine vasotocin (ADH)
due to the experimental procedure. The carrier for the steroids
was ethanol (. 02 ml/min) which is known to depress ADH secre-
tion in mammals.

Kleeman _ei_a_l. (1958) and Raisz _e_tal. (1957) sug-
gested that high doses of glucocorticoids decreased the perme-
ability of the distal nephron to water in the absence of ADH. In
the experiments presented here the corticosterone (a glucocorti-
coid) could have been acting at the distal nephron since the

experimental procedure may have depressed ADH secretion.

Reab H20 (‘70)-

98

97

96

95

57

  

OControl
" Aldos terone
0Corticosterone

r=.995

y = 99.96 - .047x

 

20 4o 60 ' so 100
V(pl/min/kg)

Figure 9

Relationship between urine flow rate and
water resorption in control, aldosterone
and corticosterone treated roosters in
Experiment 2

58

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60
TABLE 6

The Effects of Corticosterone Infusion
Rate on Glomerular Filtration Rate
for 95 Minutes ‘b

GFR (ml/min/kg) Corticosterone,“

 

 

 

Minutes
N 0-30 30-50 55-75 75-95
Control 5 1.40:.11 1,433.10 1.461: 07 1.61:.10

3. Org/min 4 1. 55?. 09 1. 5829.20 1.46:. 08 1. 36:”. 12
6. O/Ag/min 5 1,443.11 1.62:. 24 1. 88:. 20 1.60:.17
a

#0}: b ab
9.0,«g/min 4 2,272.16aL 2.12:.20 3.05123 2.67116

12.0pg/min 4 1.211.12 1.343312 1.401219 1.441120

 

d;

I“
Data presented as meanl'standard error.

>}<>}<
Means within treatments with differing superscripts

significantly different (p < . 05).

6 1
TABLE 7

The Effects of Aldosterone Infusion
Rate on Glomerular Filtration Rate
for 95 Minutes *
GFR (ml/min/kg) Aldosterone

 

 

 

Minutes
N 0-30 30—50 55-75 75-95
Control 5 1.401111 1,433.10 1.463107 1. 612. 10

0.04flg/min 4 1.39t13 1.68:.23 1.65:.12 1.53109
0.08 pg/min 5 1.441209 1.58120 1,491.16 1.383. 13
0.12,.g/min 5 1.413.07 1.34107 1.47:.25 1.27:.08

0.16Iug/min 5 1.36:.07 1.34:.09 1.25:.06 1.361106

 

>kSee footnote, Table 6.

62
TABLE 8

The Effects of Aldosterone (. 35 mg/kg/day) and

Corticosterone (14. 0 mg/kg/day) Administered

for Three Days on Glomerular Filtration Rate,
Urine Flow Rate, Water Resorption, Urate
Excretion Rate, and Body Weight Changeszk

 

 

Control Corticosterone Aldosterone
n = 4 n = 3 n = 3
afic}: b 61
AB. W. (kg) . 0251'. 044 -. 0731'. 045 . 0971’. 057
GFR
(ml/min/kg) 1.95 2.49 2.163’ . 12 2.04! .23
Reab H O(%) 99. 33 : .18X 96. 41 t 1. 22V 99.43 1.17X
2

V (,61/m1n/kg)12.4t 1.7 76.2!21.5 11.6- 3.7

Solid urine
(mg/30 min) 59.11“ 1.9 77.4!58.6 45.017.8

 

"‘Data presented as mean? standard deviation.

>”Means within parameter with differing superscripts
significantly different a and b (p (. 05), and x and y (p < . 01).

63
TABLE 9
The Effects of Corticosterone Infusion Rate

on Urine Flow Rate for 95 Minuges
V (fil/min/kg) Corticosterone

 

 

 

Minutes
N 0-30 30—50 55—75 75-95
Control 5 25.6f4.8 21.1: 5. 2 24.6 14.8 23.8 354.8

3.0‘pg/min 4 20.0144 19.9124 22.7129 24.6I1.9

6.0’1g/min 5 14.0213 12611.6 16.8128 12521.7
a>:<>:< ab b ab

9.0,..g/min 4 18.4t2.0 20.82 3.1 41.93121 38.3:11.2

c b
12.0/‘g/min 4 29.138.7a 57.6'."18.9b 81.4128.7 57.4126.8

 

I

“See footnote, Table 6.

szee footnote, Table 6.

64
TABLE 10
The Effects of Corticosterone Infusion Rate

on Water Resorption for 95 Minutes
Reab H20 (07o) Corticosterone".<

 

 

 

Minutes
N 0-30 30-50 55-75 75-95
Control 5 98. 003.41 98.46 $.39 98.24 t. 36 98.35 t .40

3. 0pg/min 4 98. 56:. 37 98.64 t. 25 98. 381‘: .29 98. 05 3.25
6. Oflg/min 5 99. 02:. 08 99.11 r.09 99.08 t . 10 98.84 2.14
9.0,.g/min 4 99. 191‘. 07 99.00: .13 98.53: .46 98.57 3.39

*>k c ab
12.0,ug/rnin 4 97.633.68a 95.90:1.21b94.61:1.47 96.61t1.23

 

>fiSee footnote, Table 6.

“See footnote, Table 6.

65

TABLE 11

The Effects of Aldosterone Infusion Rate
on Urine Flow Rate for 95 Minutes

V (pl/min/kg) Aldosterone*

 

 

 

 

 

Minutes

N 0-30 30-50 55-75 75-95
Control 5 25.614. 8 21. 1:5. 2 24.6:‘4. 23.8 i 4
0. 04,.g/min 4 28. 3:7.4 33. 8210.6 33. 3:9. 39. 3:10.
0. 08,4g/min 5 27. 5:3. 6 28. 5:4. 9 33.437. 32. 0 t 5
0.12,.g/min 5 19.4321 17.421. 9 19. 021 23. 0! 2
0.16I4g/min 5 16. 8:1. 3 16. 821.1 19.223 24.1: 4
Mean 23. 5a)”: 23. 5a 25. 9aLlD 28.4b

 

>I<See footnote, Table 6.

>MSee footnote, Table 6.

66
TABLE 12
The Effects of Aldosterone Infusion Rate

on Water Resorption for 95 Minutes
Reab H20 (07o) Aldosterone*

 

 

 

 

Minutes

N 0-30 30—50 55-75 75-95
Control 98.00241 98.46239 98.24236 98.36240
0.04Iug/min 98.18232 98.15242 98.09:.42 97.62248
0.08/Jg/min 97.86235 97.90248 97.21289 97.17275
0.12,.g/min 98.65210 98.69213 98.23249 98.16226
0.16,.g/mln 98.76208 98.69214 98.422 34 98.24231

>}<>{< b

Mean 98. 29ab 98. 38aL 98. 04a 97. 90b

 

>fiSee footnote, Table 6.

>MSee footnote, Table 6.

67
Another interpretation of these data is that the corticosterone
affected a change in the distribution of renal blood flow away
from the nephrons with 100ps of Henle to those with none.
Alternative hypotheses include the direct inhibition of ADH
release, decreasing the renal medullary osmotic gradient, and
increasing electrolyte excretion. However, there is evidence in
man that glucocorticoids do not effect ADH release (Kleeman e_t
_a_1. , 1964). In adrenalectomized rats the glucocorticoids are
necessary to re-establish the lowered medullary osmotic
gradient (Crabbe and Nichols, 1959) but adrenalectomy in the
chicken has no effect on urine flow (Brown e_ta_1. , 1958b). It will
be shown by subsequent data that corticosterone had some con-
tradictory effects on sodium excretion.

Sodium and potassium excretion

 

There was a significant interaction (level of hormone
x time) effect on the measures of sodium excretion (ENa, %ENa
and CNa) when corticosterone was infused (Table 3). In the
second experiment corticosterone had significant effects on
sodium excretion (Table 5). These data are presented in Tables
13, 14, 15, and 19.

The rate of sodium excretion (ENa) showed signifi-
cant increase by 55-75 minutes after corticosterone infusion at
3, 6 and 9 pg/min was initiated (Table 13). This response may

have been transient since ENa declined during the 75-95 minute

The Effects of Corticosterone Infusion Rate
on the Excretion Rate of Sodium for

68

TABLE 13

 

 

 

95 Minutes
ENa (ueq/min/kg) Corticosterone":
Minutes
N 0-30 30-50 55—75 75-95
Control 5 1.60221 1.33226 1.44212 1.97224
>:<::< bC
3.0pg/min 4 0.77208aL 1.022255”1.76237C 1.67243
b ab
6.0/Ag/min 5 1.55218aL 1.62225a 2.3023061 2.07226
ab b a
9.0,tg/m1n 4 1.37224a 1.58239 2.24242 1.30224
12.0pg/min 4 1.92243 1.77234 1.75247 1.63248

 

>kSee footnote, Table 6.

'wSee footnote, Table 6.

69
TABLE 14
The Effects of Corticosterone Infusion Rate

on the Clearance of Sodium for 95 Minutes
CNa (pl/min/kg) Corticosterone"

 

 

 

Minutes
N 0-30 30—50 55-75 75-95
Control 5 100112 83315 9117 125116
b

>§<>§< b
3. Opg/min 4 501551 6621561 1133222C 107226 C
b b
6. 0 pg/min 5 1041:12511 109::18a 154121 13911961
. a a b a
9. OFg/min 4 99318 115330 163332 94:18

12.0’ug/min 4 115125 105320 105328 973528

 

>kSee footnote, Table 6.

>:OkSee footnote, Table 6.

70

TABLE 15

The Effects of Corticosterone Infusion Rate
on the Percent of Filtered Sodium
Excreted for 95 Minutes
”/oENa Corticosterone*

 

 

 

Minutes
N 0—30 30-50 55—75 7595
Control 5 0.71:.06 0.589. 09 0.641: 06 0.831214
3. 0 ,ug/rnln 4 0. 331-. 04a**0. 451:. 11ab 0. 81:. 17b 0. 82:. 19b
6.0/ug/min 5 0.73:. 08 0.72:.10 0.83:.09 0.861. 07
9.0,«g/min 4 0.43: 07 0,552.13 0.581.12 0,371.08
12. OIug/min 4 0. 921:. 18 0.781.11 0. 721.12 0.621.11

 

J;
r‘s

>kSee footnote, Table 6.

«I
"See footnote,

Table 6.

71
period. This was particularly evident at the 6 and 9 tog/min

treatments. C Table 15) followed the same trends as ENa

Na(

since PNa was not affected by the steroids. When the excretion
of sodium is weighted relative to filtration rate (%ENa) only the
3 pg/min corticosterone treatment exhibited a significant
increase (Table 14). The observation that in treatments of 6
and 9 pg/min of corticosterone ENa increased as does GFR
suggest that in the rooster the excretion of sodium may be
directly effected by the GFR. One of the roles of glucocorticoids
in mammalian renal function is the maintainence of G-T balance
(Lockett, 1972). In the mammalian kidney changes in filtered
load of sodium (and GFR) are balanced by changes in proximal
tubular resorption of sodium and water (Klahr and Slat0polsky,
1973). The increase in all measures of sodium excretion (ENa,
O76ENa, and CNa) when corticosterone is infused at 3 rug/min is
indicative of inhibited sodium reabsorption at low dose levels.

In contrast to the results of the acute experiment (1),
a higher dose of corticosterone given over three days caused a
decrease in sodium excretion in liquid, solid (urates) and total
urine (Table 19). In large quantities corticosterone and cortisol
administered to ducks (Holmes and Adams, 1963) and DCA, but
not cortisone acetate, administered to cockerels (Brown $11. ,

1958a) decreased sodium excretion. Cortisone acetate had a

naturetic effect. It is important to note that, given these

72
experimental conditions, the liquid urine ENa accurately reflected
the total urine ENa' since the first experiment measured the
former only. McNabb £31: (1973) speculated that cation-urate
interactions could play a significant role in cation excretion,
particularly when challened with a large osmotic load. This
probably partially accounts for the observation by Skadhauge and
Schmidt—Nielsen (1967a) that the dehydrated rooster reabsorbs
more filtered water at a given urine: plasma osmotic ratio than
does the mammal.

In the first experiment potassium excretion was not
affected by corticosterone but did show an experimentwide
tendency to increase (p 4 . 05) during the experimental period
(Tables 3 and 20). This tendency disappeared when EK was
corrected for PK (Table 21) and GFR (Table 22) indicating that
the EK trend was probably the result of increasing PK during the
experiment. However, after three days of corticosterone treat-
ment (Experiment 2) EK (total urinary and liquid urine) was
significantly increased.

This is in agreement with the work of Holmes and
Adams (196 3) in the water-loaded duck treated with large doses
of glucocorticoids (cortisone and corticosterone). However,
Brown e_t__a_._l_. (1958a) reported contrasting effects on potassium
excretion in cockerels treated with DCA (decrease) and cortisone

acetate (increase).

73

None of the measures of sodium excretion show any
significant effects due to hormone treatment, time or their inter-
action in Experiment 1 (Tables 4, 16, 17 and 18). The most
probable explanation being that the latency period was longer
than 95 minutes in the chicken. These have been variously
reported between 30-120 minutes (see Lockett, 1972; Knochel
and White, 1973). When aldosterone was given in larger doses
(Experiment 2) a significant decrease in sodium excretion was
observed (Tables 5 and 19). The rate of sodium excretion
reported here is in close agreement with that published for the
duck (Holmes and Adams, 1963) and the male chicken (Brown
_e_t__a_l_. , 1958a, 1958b; Skadhauge and Schmidt-Nielsen, 1967a).

In the duck, Holmes and co-workers (1961, 1963) observed sig-
nificant sodium retention when aldosterone was administered.

An antinaturetic effect was observed in cockerels with DCA
treatment (Brown 2331. ,l958a). Brown e_ta_1. (1958b) noted a
decrease in sodium excretion in adrenalectomized chickens which
could be corrected by cortisone acetate but not DCA.

The effects of aldosterone on potassium excretion
during the first 95 minutes after intravenous infusion begins are
difficult to interpret. The ANOVA indicates there is a signifi-
cant level of hormone over time effect (interaction) on EK and CK
(Table 4). The 0. 08 and 0. 12 pg/min treatments showed signifi-

cant, and the control treatment showed nearly significant

 

74
TABLE 16
The Effects of Aldosterone Infusion Rate on

the Excretion Rate of Sodium for 95 Minutes
ENa (pq/min/kg) Aldosterone”

 

 

 

Minutes
N 0-30 30—50 55—75 75-95
Control 5 1. 602. 21 1. 331:. 26 1.441. 12 l. 971:. 24
0.04Ag/min 4 Z.18t.63 2051.75 2943.94 2781.81
0. 08 pg/rnin 5 2. 911:. 78 2. 889.. 77 2. 76:.69 2. 793.. 88
0.12/cg/min 5 0. 80:. 16 0. 872 19 0. 871.16 0. 90:. 16
0.16;:g/rnin 5 1. 54:. 19 1.631. 15 1. 701». 25 1. 301:. 19

 

>kSee footnote, Table 6.

 

 

75
TABLE 17
The Effects of Aldosterone Infusion Rate on

the Clearance of Sodium for 95 Minutes
CNa (pl/min/kg) Aldosterone*

 

 

 

 

 

 

 

Minutes
N 0-30 30-50 55-75 75-95
Control 5 100112 83315 91 f 7 125316
0. 04 Aug/min 4 1613241 1581' 52 2341175 229174
0. 08,1g/min 5 191345 189144 185138 185152
0.12/4g/min 5 48 i 9 521'11 52310 54110
0. l6flg/min 5 103113 109310 1131’17 881'13
>kSee footnote, Table 6.
TABLE 18
The Effects of Aldosterone Infusion Rate on
the Percent of Filtered Sodium Excreted
for 95 Minutes ..
%ENa Aldosterone'"
Minutes
N 0-30 30-50 55-75 75-95
Control 5 0. 712 06 0.58209 0. 642 06 0.83214
0.04pg/min 4 1.041121 0.88128 1. 331'. 44 1.421'. 47
0.08/4g/min 5 1.571.41 1.441“. 39 1.461. 42 1.501.42
O. lZflg/min 5 0 331’. 06 0. 371’. 07 0 521' 23 0. 431. 08
0. l6/Ag/min 5 0.771 10 0.85:.09 0.95.! 16 0.64:.08

 

>kSee footnote, Table 6.

 

76
TABLE 19

The Effects of Aldosterone (0. 35 mg/kg/day)
and Corticosterone (l4. 0 mg/kg/day)
Administered for 3 Days on the Excretion
Rates of Sodium and Potassium in Liquid,
Solid and Total Urine, and Liquid Urine"
Concentration of Sodium and Potassium,“

 

 

 

 

 

Control Corticosterone Aldosterone
n : 4 n = 3 n : 3
:10}: b
UNa (meq/l) 187.8350. la 15.913.2b 70.2315.7
UK (meq/l) 68.41319 41.1316.2 81.5!32.7
Liquid Urine
ENa a ab b
(peg/30 min/kg) 68. 3318. 8 35. 214. 3 24. 318. 9
EK b a
(peq/3O min/kg) 25.02122a 82438.3 26.7320
Solid Urine
ENa x
(peq/30 min/kg) 12026.0 1.310. 7y 2820.1Y
EK
(peq/30 min/kg) 15.6227 13.21145 9.726.3
Total Urine
ENa b b
(peq/30 min/kg) 82. 31’24. 4a 36. 513. 6 27. 13 9. 0
E
K . a b a
(yeq/30 min/kg) 40.6“!17.5 103.91'27. l 36.5313.3

 

>'zData presented as mean 3 standard deviation.

**Means within parameter with differing superscripts

are significantly different, a and b (p < . 01), and x and y (p < . 05).

77
TABLE 20

The Effects of Corticosterone Infusion Rate
on the Excretion Rate of Potassium
for 95 Minutes
EK (peq/min/kg) Corticosterone,"

 

 

 

Minutes
N 0-30 30-50 55-75 75-95
Control 5 0. 343. 03 0. 382. 04 0. 531. 07 0. 821. 13

3.0)Ag/min 4 1.073.18 0.971320 0.921.20 0.771315
6. Opg/min 5 0. 982.19 0. 893. 09 1. 261. 20 1.423.11
9.0pg/min 4 1.062.27 1.313.33 1.531.36 1.281342

12.0}tg/min 4 0.68207 0.78209 0.81206 0.88213

 

a :1: >1: ab ab b

Mean 0.81 0.84 1.00 1.04

 

\\\\\

IIIII See footnote, Table 6.

78
TABLE 21

The Effects of Corticosterone Infusion Rate
on the Clearance of Potassium for 95
Minutes
CK (,J/min/kg) Corticosterone'

 

 

 

 

Minutes

N 0-30 30-50 55-75 75-95
Control 5 921 6 103 I 9 133314 215133
3. OPg/min 4 261148 250251 22343 178134
6. 0,ug/rn1n 5 258142 244139 311245 343126
9. OFg/min 4 2971-72 366287 433195 320192
12.0,..g/m1n 4 222120 244122 247225 2661'51

*See footnote, Table 6.
TABLE 22

The Effects of Corticosterone Infusion Rate
on the Percent of Filtered Potassium
Excreted for 95 Minutes
%EK Corticosterone*

 

 

 

Minutes
N 0.30 30-50 55-75 75-95
Control 5 6. 91:0. 6 7. 6‘10. 9 9. 5:1. 2 14. 0:2. 2
3. Orig/min 4 17. 313.0 17.613. 7 14.812. 3 12. 8:2. 2
6. ofig/min 5 18. 912. 8 17.7128 18. 22:2. 8 24. 1:2 9
9. opg/rnin 4 12. 222. 5 17. 41:3. 8 14. 313.2 11. 3:2. 9
12.0,.g/min 4 20.623. 0 20. 023.4 20.0229 19.6329

 

("See footnote, Table 6.

79

(p < . 10), time related effects for EK' InSpection of the data in
Tables 23 and 20 indicates that in the control birds EK and CK
began increasing during the 55-75 minute period and continued
until the end of the experiment whereas the 0. 08 lug/min treat-
ment caused an increase at the 55-75 minute period and began
declining during the 75-95 minute period, and the 0. 12 fig/min
began decreasing during the 30-50 minute period becoming
significant at the 55-75 minute period, and starting to rise dur-
ing the last period. When expressed as a percent of filtered load
(%EK) the interaction effect becomes nonsignificant (Tables 4 and
15). In Experiment 2 where aldosterone was administered for
three days there was no significant effect on potassium excretion
(Tables 5 and 19). These two experiments taken together led to
the conclusion that aldosterone had no permanent effect on
potassium excretion in the male chicken. Aldosterone treatment
in ducks (Holmes and Adams, 196 3) and DCA treatments in
cockerels (Brown e_ta_1. , 1958a) had the astonishing effect of
decreasing potassium excretion. But, Brown e_ta_1. (1958b)
observed no effect on potassium excretion in the adrenalecto-
mized male chicken.

The role of aldosterone in the renal excretion of
sodium and potassium has been the subject of intensive research
efforts during the past haventy years, particularly in mammalian

species. Typically, aldosterone promotes sodium reabsorption

80
TABLE 23

The Effects of Aldosterone Infusion Rate on
the Excretion Rate of Potassium for 95
Minutes >2
EK (keg/min/kg) Aldosterone"

 

 

 

Minutes
N 0-30 30-50 55-75 75-95
Control 5 0. 34!. O3 0. 381'. 04 0. 531’. 07 0. 821. 13

0.04,.g/min 4 1.043220 0.891218 1.381223 1.191118

0.08/4g/min 5 0.77.2076"‘°"‘0.76.’:.068L 1.19.2231) 1.10220aLb

ab b ab

0.12,.g/m1n 5 1.452152:1 1.24208 0.97212 1.07217

0. l6,ug/min 5 0.641.08 0.611109 0.713.13 0.53106

 

 

>kSee footnote, Table 6.

>“(See footnote, Table 6.

81
and potassium excretion (Lockett, 1972; Knochel and White, 1973).
Aldosterone exerts its effect primarily on the distal tubule of the
nephron (Knochel and White, 1973; Schultze, 1973). These authors
concluded that there is a dissociation of effects of aldosterone on
sodium and potassium transport and that it is not an exchange of
sodium for potassium or hydrogen as was formerly thought. In
line with this hypothesis, Malnic _e£_al. (1966), based on their
microPuncture studies, proposed that there was an active
resorption of sodium and potassium, and passive secretion of
potassium in the distal tubule. They state that the direction and
rate of potassium movement was determined by the balance of
these forces. It has also been postulated that a difference in
function may exist between the early and late distal tubule (Burg
and Stoner, 1974). The data support the concept of separation of
sodium and potassium effects. In the chronic experiment
(Experiment 2) sodium retention was increased and potassium
excretion unaffected. When aldosterone was infused at levels
near estimated physiological secretory rates (Experiment 1)
potassium excretion was sometimes affected (in one case
positively and in the other negatively) without change in sodium
retention up to 95 minutes. Permanent effects on the sodium
retention may have been missed because the latency period for
aldosterone action may have been longer than 95 minutes.

Lonsdale and Sutor (1971) demonstrated that the solid

 

82
portion of the bird urine consists of irregular layers of uric acid
dihydrate and trapped soluble materials. McNabb e_til: (1973)
reported between 40 and 75 percent (depending on dietary protein
level) and 20 percent of the total excreted sodium and potassium,
respectively, was contained in the precipitated fraction of urine
in the rooster. It was found that less sodium and more potassium
(depending on treatment) were excreted (percentagewise) in the
precipitated urine in Experiment 2 (Table 26) than was observed
by McNabb. The most probable explanation for the lower
percentage of sodium is that the dilution of the urine with
deionized distilled water at the time of collection prevented the
sodium from being trapped in the soluble layers between layers
of uric acid crystals as McNabb and his collaborators have
suggested. The data indicates that significantly less sodium and
potassium, percentagewise, were excreted in the solid phase of
the urine after corticosterone treatment (Table 26). From the
data of McNabb e_ta_l.(l973) there appears to be an inverse rela—
tionship between the liquid phase of urine sodium and potassium
concentration, and percentage excreted cation in the precipitate.
This is contrary to results of Experiment 2 (Tables 19 and 26).
The corticosterone treated birds had the lowest urine sodium and
potassium concentrations and very low solid phase sodium and
potassium excretion; the solid urine response to corticosterone

treatment was highly variable but not significant. This would

 

83
occur if urine hydrogen ion (or ammonium ion) concentration
increased. Urate has a higher affinity for these cations than for
sodium or potasiurn (Porter 1963a, 1963b). Therefore, it is
possible that corticosterone increased acid excretion.
TABLE 24
The Effects of Aldosterone Infusion Rate on

the Clearance of Potassium for 95 Minutes
CK (pl/min/kg) Aldosterone’k

 

 

 

 

Minutes
N 0-30 30-50 55-75 75-95

Control 5 92 L’.’ 6 103 1 9 133114 215133

0. O4 pg/min 4 252253 214240 325139 262335
a>2<>.'< ab b ab

0. 08 lug/min 5 242134 258125 3563582 284353
b ab

0.12,.g/m1n 5 38214961 328 1'19ab 250134 259333

0.16,.g/m-1n 5 158115 150118 177330 133314

 

*See footnote, Table 6.

(”See footnote, Table 6.

 

84
TAB LE 25

The Effects of Aldosterone Infusion Rate on
the Percent of Filtered Potassium Excreted
for 95 Minutes '
% EK Aldosteronea<

 

 

 

 

Minutes
N 0.30 30-50 55-75 75-95
control 5 6. 920.6 7.610. 9 9. 511.2 14.0122

0. 04pg/min 4 18. 533. 5 13.612. 5 20.4127 17.2322
0. 08/tg/min 5 17. 2:22 18. 511. 9 24. 314.5 19. 913.2
0.12’ug/min 5 26.6124 25. 111.7 19.7123 20.6‘226

0.16pg/min 5 ll.7‘.*.'0.9 ll.5'.".1.2 14. 512.9 9.73.0.8

 

>kSee footnote, Table 6.
TABLE 26

The Effects of Aldosterone (0. 35 mg/kg/day) and

Corticosterone (l4. 0 mg/kg/day) Administered for

3 Days on Percent of Total Sodium apd Potassium
Excreted in Solid Urine“

 

 

Control Aldosterone Corticosterone
n I 4 n 2 3 n : 3
>:<>:< b
Na 15. 234. 2a 11.113. 561 3. 7:2. 3
b b
K 39. 237. 861 24.519151 11. 139. 7

 

>i‘See footnote, Table 8.

>M‘Means within parameter with different superscripts
are significantly different (p < . 01).

 

CONCLUSIONS

1. Glomerular filtration rate (GFR) shows consider-
able variability between and within individual roosters.

2. Corticosterone at estimated physiological
secretory rates can increase GFR at least transiently.

3. Aldosterone has no short term or long term
effects on GFR.

4. Corticosterone can create a diuresis by increas-
ing GFR or decreasing water resorption.

5. Aldosterone does not alter urine flow rate or
water resorption.

6. Corticosterone has a short term naturetic effect
which is attributable to increases in sodium filtration rates and
decreases in sodium resorption.

7. Corticosterone, chronically administered, has an
antinaturetic and kaluretic effect which is most probably associ-
ated with increased excretion of hydrogen and ammonium ions.

8. Aldosterone, chronically administered, has an
antinaturetic effect but no kaluresis is observed.

9. Aldosterone can cause contrasting results,

85

86

depending on dose, up to 95 minutes after administration on
potassium excretion, but sodium excretion is not affected during
this time indicating that the latency period for aldosterone action
may be longer than 95 minutes.

10. The data support the concept that sodium reten-
tion and potassium secretion are not linked in the distal tubule.

11. Liquid urine excretion rates of sodium and

potassium reflect total urine excretory rates.

LITERATURE CI TED

Acher, R. , 1971. The neurohyp0physeal hormones--An
example of molecular evolution. In Biochemical Evolution
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Akester, A. R. , 1964. Radiographic studies of the renal portal
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Akester, A. R. , 1967. Renal portal shunts in the kidney of
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Akester, A. R., R. S. Anderson, K. J. Hill, and G. W.
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August, J. T., D. H. Nelson and G. W. Thorn, 1958. Response
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Bayle, J. D., J. Boissin, J. Y. Daniel, and I. Assenmacher,
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Bean, J. W., 1942. Specificity in the renin-hypertensinogen
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Benoit, J., 1950. Traite de Zoologie, edited by P. P. Grasse,
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Bessonov, B. I. , 1972. Electr0physiological study of function of
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Bhattacharyya, T. K., A. K. Sarkar, A. Ghosh, and A.
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87

88

Bindslev, N. , and E. Skadhauge, 1971. Salt and water perme-
ability of the epithelium of the coprodeum and large intes-
tine in the normal and dehydrated'fowl (Gallus domesticus).
In vivo perfusion studies. J. Physiol. , 216:735-751.

 

Bindslev, N., and E. Skadhauge, 1971b. Sodium chloride
absorption and solute-linked water flow across the
epithelium of the cOprodeuIn and large intestine of the

normal and dehydrated fowl (Gallus domesticus). In vivo
perfusion studies. J. Physiol. 216:753-768.

 

Boissin, J. , 1967. Le Controle hypothalamo-hypophysaire de la
fonction cortico-surrenalienne chez le canard. J. Physiol.
(Paris) 59:423—444.

Boissin, J., J. D. Bayle, and I. Assenmacher, 1966. Le
fonctionnement cortico-surrenalien du canard male apres

prehypophycsectomie ou autogreffe hypOphysaire ect0pique.
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Bokori, J., 1961. Acta Vet. Med. Hung. 11:415-422.

Bouille, C., and J. D. Bayle, 1973. Experimental studies on
the adrenocorticotropic area in the pigeon hypothalamus.
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APPENDIX

Clearance Data Experiment _1_

 

TABLE 1

Cortic os ter one
GFR (ml /min /kg)"‘

 

Minutes Control 3. 0 6. O 9. O 12. 0
pug/min pg/min pg/min Pg/min

 

 

 

0-10 1.36:.12 1,743.24 1,433.08 2.08:.24 1.041.23
(5V= (4) (5) (4) (4)
10-20 1.37:.27 1.45:.10 1,431.27 2.49:.23 1.25:.18
20-30 1,473.19 1.46:.08 1,463.23 2.253.35 1.36:.21
30-40 1.39: 18 1,311.25 1.47:.32 1,863.25 1,353.15
40-50 1.47:.12 1.85:.27 1.77:.38 2.39:.26 1.341.22
55-65 1.43:;08 1,431.09 1.83:.33 3.143.37 1.41:.30 {
65-75 1,492.14 1,491.14 1.94:.26 2,961.33 1.38:.28
75-85 1.603217 1,203.17 1,682.20 2.44:.16 1.442.28
85-95 1.62:.14 1.51:.16 1,513.31 2.91:.24 1.45:.32 '
P NS NS (.10 (.05 NS K

 

>kMeant Standard Error (11).

101

102
TABLE 2

Corticosterone
V (#1 /min/kg )*

 

 

3. O 6. 0 9. 0 12. 0
Minutes Control pg/min pg/min pg/min pkg/min

 

 

 

0-10 29.6310.619.229.9 14.011.8 17.2:3.1 31.4319.9
(5H< (4) (5) (4) (4)

10-20 23.416.7 21.4:8.3 13.9:2.0 19.2:4.1 28.8:16.2
20-30 23.928.7 19.416.4 14.113.2 18.714.1 27.1113.3
30-40 22.328.2 20.2:6.4 13.612.3 20.1:4.6 41.4116.3
40-50 19.917.3 19.7:3.5 13.612.5 21.514.8 73.8135.0
55-65 23.616.3 18.8!2.8 15.813.3 41.2115.581.4!46.1
65-75 25.538.0 26.6:4.6 18.0:1.8 42.7:21.281.4:46.4
75-85 24.018.0 26.3:2.8 18.3:1.9 42.4219.969.3:45.1
85-95 23.7:7.2 22.812.6 16.623.1 34.2113.153.6I36.1
P NS NS NS <. 05 4 05

 

 

*See Table 1.

 

103

 

 

 

 

TABLE 3
Corticosterone
Reab H20 (%)>:<
3.0 6.0 9.0 12.0
Minutes Control y-g /min p g/min p g/min p. g/min
1-10 97.63 98.68 99.02 99.16 96.94
1.96 1.82 1.13 't.14 21.74
(5)* (4) (5) (4) (4)
10-20 98.11 98.39 98.98 99.22 97.87
1.63 1.75 1.14 1.17 21.03
20-30 98.27 98.61 99.06 99.18 98.09
1.65 1.53 1.15 1.10 1.85
30-40 98.36 98.46 99.02 98.95 97.09
1.60 73.41 1.14 1.15 31.04
40—50 98.56 98.82 99.19 99.06 94.72
1.56 1.32 1.13 1.24 12.18
55—65 98.31 98.70 99.15 98.65 94.46
3.46 1.15 1.13 1.47 12.16
65-75 98.16 98.07 99.01 98.41 94.75
1.61 1.55 1.15 3.87 12.32
75-85 98.16 97.66 98.88 98.31 96.47
1.6u. 1.38 1.11 1.72 12.05
85—95 98.38 98.44 98.80 98.83 96.74
1.61 1.21 1.28 1.42 11.69
P NS NS NS NS (.05

 

>kSee Table 1.

104

TABLE 4

Corticosterone

ENa (peq /min /kg)*

 

 

 

3.0 6.0 9.0 12.0
Minutes Control pg/min ug/min pug/min pg/min
0-10 1.851.49 0.821.11 1.701.36 1.52:.47 1.951.83
(5H= (4) (5) (4) (4)
10—20 1.401.34 0.691.15 1.50:.31 1.47: 51 1,861.71
20—30 1.561.31 0.781.19 1.461.31 1 131.33 1,941.91
30—40 1.33:.23 0.92:.37 1.471.14 1.561.55 1.761.46
40-50 1.32:.50 1.132.39 1.77:.49 1.601.64 1.761.57
55-65 1.351.17 1.571.51 2.651.52 2.081.52 1.891.73
65-75 1,541.17 1,951.59 1.961.29 2.401.72 1.62:.70
75-85 1.821.36 1.571.56 2.20:.42 1.29:.37 1.671.77
85-95 2,121.34 1.761.75 1.94:.36 1.311.38 1.581.69
P NS (. 05 <. 05 (.05 NS

 

*See Table 1 .

 

105

 

 

 

 

TABLE 5
Corticosterone
WOEN:
3.0 6.0 9.0 12.0
Minutes Control pg/min pg/min pg/min pg/min

0-10 0.843.16 0.34: 07 0.771.16 0,531.15 1.051.40

(5)* (4) (5) (4) (4)
10-20 0.631.06 0.321.08 0 731 14 0,431.15 0.861.25
20-30 0.66:.08 0.34:.06 0.70:.13 0 341.07 0 84: 34
30-40 0.61:.09 0.461.15 0,741.11 0,581.19 0.80:.20
40-50 0.541;16 0.45:.18 0,711.17 0.53:.22 0.761.14
55-65 0.59:.07 0.711.20 0.97:.12 0,531.17 0.781.19
65—75 0.68: 11 0.911.29 0.691.10 0.631.19 0.661.17
75-85 0 76* 20 0.861.28 0.861.13 0.391.12 0.611.18
85-95 0 901.22 0.781.29 0.87:.07 0.34:.11 0.62:.17

P NS (.05 INS NS NS

 

>*‘See Table 1.

 

 

 

106
TABLE 6

Corticosterone '
CNa (pd/min/kg)

 

 

 

3. 0 6. 0 9. 0 12. 0
Minutes Control pg/min pg/min pug/min rug/min
0-10 115327 54307 113125 109334 116349
(5)* (4) (5) (4) (4)
10-20 87119 46310 101123 106138 114.142
20-30 98:18 51312 97:21 821125 116153
30-40 84313 50:22 98:12 113143 105327
40-50 82328 73:23 120135 117349 105133
55-65 85310 1011130 177137 150140 113143
65-75 97.111 126136 131120 175156 97:41
75-85 115323 1011' 34 147130 93128 100146
85-95 135123 113345 130127 95329 951’41
P NS <. 05 <. 05 C. 05 NS

 

>i‘See Table 1.

 

 

 

 

107
TABLE 7

Corticosterone .
EK (Peg/min /kg)

 

 

3. 0 6. 0 9. 0 12. 0
Minutes Control H- g/min pg/min pg/min jug/min

 

 

0—10 0.35:.04 1.09:.35 1.171.56 1.131.62 0.601210
(SPk (4) (5) (4) (4)

10—20 0,281.04 0.991.33 0.841.12 1.071.46 0.721.14
20—30 0.391.05 1.121.35 0.931.15 0.991.44 0.711.17
30-40 0.401:06 0.951.31 0.861.07 1.321.54 0.801.16
40-50 0.36:.07 0.991.31 0.911.18 1,311.48 0,761.12
55-65 0.451.06 0.931.36 1.071.27 1.581.61 0.801.07
65—75 0.621.12 0.921.25 1.45:.30 1.47:.47 0.821.11
75-85 0.741.19 0.721.22 1.49:.19 1.13:.52 0.84:.18
85-95 0.91:.20 0,823.24 1.361.14 1.43:.72 0.92:.22

 

 

>i‘See Table l .

—————-_.

 

   

108

 

 

 

TABLE 8
Corticosterone
O/OEK *
3.0 6.0 9.0 12.0
Minutes Control pg/min pg/min r-g/min pg/min
0-10 7.41.9 16.91%.3 18.636.7 14.036.3 21.415.6
(5)::< (4) (5) (4) (4)
10-20 5.81.7 16.535.0 18.234.4 11.033.4 21. 316.2
20-30 7.631.2 18.535.8 20.124.3 11.713.7 19.015.1
30-40 8.5.21.5 19. 3135.2 18.633.7 19.035.5 18.933.9
40-50 6.7.21. 1 15.915.9 16.834.6 15.91'5.9 21. 126.2
55-65 8.221.2 15.414.5 16. 234.2 14.034.7 20.114.7
65-75 10. 912. 1 14. 1:2. 1 20. 213. 9 14. 635. 1 19. 934. 1
75-85 13. 814.0 13 53.3 9 23.533.9 11.0:4.0 18.4:3.4
85-95 14. 212. 5 12. 0'32. 8 24. 7:4. 7 11. 734. 9 20. 8'55. 2
P NS NS NS NS NS

 

>=<See Table 1.

 

 

109

TABLE 9

Corticosterone

CK ( 1/min/kg)*

 

 

 

3. 0 6. 0 9. 0 12. 0
Minute 3 Control pg/min pg/min p g /min 1. g/min
0-10 96 I 8 270 198 2851119 3241172 2031 40
(5)* (4) (5) (4) (4)
10-20 76111 240179 2311 41 295.1117 236137
20-30 103.: 13 273 1 95 259: 44 2701114 2282+. 37
30-40 112: 12 2433 79 2311 18 363:140 245 137
40-50 95 1 12 257:: 77 257: 58 3701125 242 1 30
55-65 115 1 14 230: 81 2581 58 4511164 2471 31
65-75 152 :24 215: 47 3641265 4151164 248143
75-85 199 1 49 166 1 46 3701 46 2821113 2561 68
85-95 2311 50 191: 56 316157 3571161 276185
P NS NS NS NS NS

 

* See Table 1.

 

110

TABLE 10

Corticosterone
Filtered K ( eg/min/kgf:<

 

 

3.0 6.0 9.0 12.0
Minutes Control pug/min ug/min pug/min pg/min
0-10 4.87:.56 7.25:1.005.501.67 7.11:.94 3.091161
(5H< (4) (5) (4) (4)

10-20 5.03:1.115.94 .40 5.202.84 8.72i1.093.781.65
20-30 5.7411.196.04 .45 5.33:.91 7.99:1.334.141.72
30—40 4.97:.85 5.19 1.035.373.99 6.511.00 4.40:.74
40-50 5.472.55 7.08 .99 6.2711.098.2211.064.111.63
55-65 5.591.42 5.61 1.107.183.95 10.771 4.55:.85
65—75 5.96:.73 6.27 .83 7.55:.98 10.321 4.60:;84
75-85 5.901.80 5.10 .91 6.673.60 9}8;:1.064.812.82
85-95 6.22:.51 6.39 .79 6.25:1.0010.92: 5.04:1.08

1.25

 

*See Table 1.

 

 

 

lll

Clearance Data Experiment ;

 

TABLE 11

Aldosterone

GFR (ml /min /kg ) *

 

 

 

 

0.04 0.08 0.12 0.16
Minutes Control pkg/min pg/min pg/min pg/minl
0—10 1,361.12 1,241.14 1.54:.17 1.54:;12 1.341.09
(5H (4) (5) (5) (5)
10-20 1,372.27 1.421131 1.44:.16 1 42+ 15 1.40:.13
20-30 1.47:.19 1.40:.25 1.33:.15 1.28:.09 1.33:.15
30-40 1 391.18 1.94:.41 1.60:.20 1.30+ 13 1 341 11
40-50 1 47: 12 1.421.18 1,563.37 1 383.07 1 342.16
55—65 1 431.08 1.79:.13 1.47:.15 1.41? 34 1.28:.09
65-75 1 49: 14 1,511.20 1.50:.29 1 54: 42 1.22:.10
75-85 1 601.17 1.51:.11 1,323.21 1 333.07 1 27:.12
85—95 1,621.14 1.551.17 1.43:.17 1.22:.15 1.443.04
P NS NS NS NS NS

 

*See Table l.

 

 

112
TABLE 12

Aldosterone
V (Fl/min/kg) =.<

 

 

 

 

0. 04 0.08 0. 12 0. 16
Minutes Control pg/min pg/min pg/rnin pg/min
0-10 29. 6110. 6 26.6112. 529. 8:! 8.6 23.1: 5. 0 16. 81' 2.4
(5)* (4) (5) (5) (5)
10-20 23. 41 6. 7 27. 1:13. 6 28. 7: 5. 9 18.0 1 3. 1 17. 1 z! 1. 6
20—30 23. 9:: 8.7 31.1116. 023. 91 4. 8 17. 21 2. 9 16. 7 1- 3.2
30-40 22. 3: 8. 2 32. 53.15.628.62 6. 9 17. 8: 2.6 15. 9: 2.1
40—50 19. 9: 7. 3 34.2116. 828.42 7. 9 17. 03: 3.1 17.7 1 1.1
55-65 23.6: 6. 331.6214.835.4111.4 19212.6 17. 013.5
65-75 25. 52*. 8.035. 0313.531. 32 9.51883 3.021. 3 16.1
75-85 24. 0:: 7. 2 37. 3:15. 829. 6 i 6. 0 22. 6 .t 3.6 23.3 t 6. 8
85-95 23. 7: 7. 241. 3115. 534.42 8.623.424.424. 9: 5.4
P NS NS NS NS NS

 

*See Table 1 .

113
TABLE 13

Aldosterone
Reab H20 (‘70) *

 

 

 

 

 

0.04 0.08 0.12 0.16

Minutes Control pg/min pg/min pg/min pg/min

0-10 97.63:.9698.033.7097.76:.8298.561.2098.76i.15

(5)72 (4) (5) (5) (5)

10-20 98.111.6398.33:.4597.723.7098.73:.1698.74I.18
20-30 98.271.6598.171.6298.121.3698.67t.1798.79r.11
30-40 98.361.6098.521.3898.173.4198.59:.2198.811.12
40—50 98.56:.5697.782.7697.62:.9198.79:.1798.581.26
55-65 98.311.4698.311.7297.221 97.871.9698.701.25
65—75 98.16!.6197.88$.539;:::t 98.601.2998.13z.64
75-85 98.321.5997.7lt.799;::23 98.241.3698.251.50 '
85-95 98.381.6197.53t.669;:igt 97.991.4298.24i.42

1.15

P NS NS NS NS NS

 

>}<See Table l.

 

114
TABLE 14

Aldosterone
ENa (Meg/min /kg)

 

 

 

0.04 0.08 0.12 0.16
Minutes Control pg/min pg/min pg /min I-bg/min
0-10 1.851.49 2.00:.99 3.8112.050.85:.09 1.481.38
(5V< (4) (5) (5) (5)
10-20 1 401.34 2.7211.482.84:6.170.912.41 1.50:.27
20_30 1 76: 31 1.8211.012.092;69 0.64:.28 1 631.40
30-40 1 331.23 1.733.82 3.1111.320.863.29 1.74:.20
40—50 1 321.50 2.37tl.362.643.94 0.871.27 1 521.23
55-65 1 352.17 2.68:1.483.0411.021,003.29 1 40: 18
65—75 1 541.17 3.2111.382.4911.030.74i.16 1 991.46
75-85 1 821.36 2.7511.243.1511.630.991.26 1 291.31
85-95 2 121.34 2.80t1.222.44:.88 0,803.20 1.33:.24
P NS NS NS NS NS

 

>1<See Table 1.

 

 

115

 

 

 

 

TABLE 15
Aldosterone
%ENa*
0.04 0.08 0.12 0.16
Minutes Control u-g/min [pg/min pg/min pkg/min
0-10 0.84:.16 1.111.40 1.91:1.000.342.04 0.741.21
(5)* (4) (5) (5) (5)
10-20 0.63: 06 1 273.45 1.591.71 0 37::15 0.773.22
20—30 0.66: 08 0 771.29 1.22:.47 0.29:.12 0.81:.15
30-40 0.61! 09 0.65:.28 1 38: 59 0 381.10 0.90:.14
40-50 0.54:.16 1 111.51 1 50: 57 0 372 10 0 791.13
55—65 0.59:.07 1 051.50 1 591.54 0 731.47 0,751.12
65-75 0,681.11 1 601.77 1 341.69 0 312.05 1,141.30
75-85 0.76:.20 1.34:.58 1 691.67 0.441.10 0.671.13
85-95 0.90:.22 1 511.84 1.31: 55 0,421.14 0.621.11
P NS NS NS NS NS

 

>kSee Table l.

 

 

 

116

 

 

 

 

 

TABLEzw
Aldosterone
cNa(m1/min/kg)*
0.04 0.08 0.12 0.16
Minutes Control pg/min pg/min pg/min pg/min
0-10 115127 148166 2471119 5116 99126
(5H< (4) (5) (5) (5)
10—20 87119 199196 188166 55125 100119
20—30 98118 134166 137138 39117 109127
30—40 84113 136163 203278 52118 116113
40-50 82128 181193 174152 52117 102116
55-65 85110 2041101 207153 60118 94113
65-75 97111 2631125 163160 44110 132130
75-85 115123 217198 208199 59115 86122
85-95 135123 2401126 162148 48112 80116
P NS NS NS NS NS

 

*See Table l.

 

117

TABLE 17

Aldosterone

EK (u-eq /min/kg)

 

 

 

0.04 0.08 0.12 0.16
Minutes Control ling/min pg/min pg/min gag/min
0-10 0.351.04 0.931.32 0.821.08 1.721.28 0.691.15
(5V< (4) (5) (5) (5)
10-20 0.281.04 1.261.50 0.851.16 1 521.30 0.641.14
2030 0,391.05 0,931.28 0.651.10 1,101.16 0.601.15
30—40 0.401.06 0.801.20 0.811.11 1 161.12 0.681.15
40—50 0.361.07 0.981.31 0.711.04 1 311.11 0.541.10
55-65 0 451.06 1 291 37 1 411.42 1 001.19 0.641.13
65-75 0.621.12 1.461.33 0 961 22 0 931 16 0.781.24
75-85 0.741.19 1.261 32 1 141.23 1 22+ 30 0.511.11
85-95 0.911.20 1 111.23 1 061 36 0 911.16 0.551.04
P (.10 NS <. 05 (. 05 NS

 

>1<See Table 1.

 

 

 

118

 

 

 

 

TABLE 18
Aldosterone
OZOEK *

0.04 0.08 - 0.12 0.16

Minutes Control Jag/min Jag/min pg/min pg/min

0-10 7.371.9318.401 17.151 32.011 13.261
5.10 2.93 4.09 1.85

(SVR (4) (5) (5) (5)

10-20 5.811.6523.401 19.711 27.181 10.941
9.03 5.09 4.16 1.66

20-30 7.631 13.831. 14.601 20.551 10.941
1.24 3.41 3.55 3.09 1.48

30-40 8.501 10.791- 19.011 24.501 11.9 I
1.53 3.41 1.45 3.13 1.19

40-50 6. 701 16.471 17. 981 25.68 1 11. 041
1.12 3.35 3.67 1.81 2.27

55-65 8.161 18.661 27.741. 19.67 1 11.891
1.21 3.99 7.03 2.87 1.32

65-75 10. 861 22.231 20.871 19.78 1 17.051
2.12 3.97 5.85 4.00 5.67

75-85 13.771 18.271 22.121: 20.88 1 9.79 1
4.03 3.05 3.14 4.39 1.43

85-95 14.171 16.141 16.63 1 20. 39 1 9. 63 1
2.54 2.52 5.47 3.18 0.90

P NS NS NS NS NS

 

*See Table l.

119

TABLE 19

Aldosterone

CK (“l/min/kg) *

 

 

 

0.04 0.08 0.12 0.16
Minutes Control 1‘ g/rnin ug/min ug/min ug /min
0-10 96. 31 230.51 249.7 1 511.0 1 174. 91
8.0 76.4 38.8 103.7 24.8
(5W< (4) (5) (5) (5)
10-20 76.01 325.5: 275.51 372.8 1 150.81
10.7 136.6 82.1 63.3 26.6
20—30 102.6 1 201.21 200. 31 264. 5 1 148.81
13.0 58.2 54.3 48.9 32.1
30—40 111. 9 1 188. 31 266. 31 306. 91 164. 21
14.0 42.5 30.9 33.5 30.1
40—50 94. 5 1 239.51 250.01 349.1 1 135. 21
11.6 72.1 52.2 14.7 21.3
55-65 114.81 324.61. 440.41 255 41 154571
13.7 64.8 146.8 58.7 25.3
65—75 151.91 325.51 271.71 245.0:1 198.8 1
23.9 55.4 71.7 42.7 55.7
75-85 198.81. 275.11 304.01: 278.21 127.631
48.5 61.4 71.6 59.9 264
85-95 230.81 248.31 260.81 239.31 138.21
49.5 41.5 83.7 31.7 11.3
P NS NS <. 05 <. 05 NS

 

>l‘See Table 1.

 

 

120
TABLE 20

Aldosterone
Filtered K (peq/min/kg) *

 

 

0. 04 0.08 0.12 0. 16
Minutes Control pg/min pg/min pug/min pg/min

 

 

 

0—10 4.87:.56 4.641.59 5.171.64 5,741.29 5.231.70
(5H= (4) (5) . (5) (5)
10—20 5.0311.115.3511.084.89!.75 5.9911.046.011.90
20-30 5.7411.196.4611.034.731.67 5,391.42 5.251.81
30-40 4.971.85 7.9211.914.221.38 5.061.73 5.401.70
40—50 5.471.55 5.471.87 4.611.95 5,181.42 5.121.47
55-65 5,591.42 6.451.80 4.961.37 5.5611.185.151.54
65-75 5.961.73 6.411.97 5.7411.415.8111.524.681.43
75-85 5 901.80 6.581.60 5.031.68 5.691.47 4.971.51
85-95 6,221.51 6.761.87 6.801.73 4.731.96 5.81:.44
P NS NS NS NS NS

 

*See Table l.

 

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