The activity of both sympathetic neurons in the central nervous system and peripheral sympathetic nerves that innervate the heart and blood vessels is elevated in hypertension. However it is unclear about the roles of sympathetic ganglia, which integrate central sympathetic signals and send their signals to cardiovascular end organs via sympathetic nerve. The celiac ganglion (CG) plays an important function in regulating blood pressure by the controlling splanchnic circulation containing 30% of total blood volume. Reactive oxygen species (ROS) are elevated in CG in hypertension. Ion channels, essential factors for neuronal firing, are possible targets for ROS. The purpose of this study is to find if neuronal firing and ion channels are modulated in hypertension and if ROS are related to changes in neuronal firing and ion channels in hypertension. Neuronal firing patterns were explored in dissociated CG neurons from DOCA-salt hypertensive rats. In response to sustained suprathreshold current injection, more phasic neurons, fewer adaptive neurons and tonic neurons were shown in dissociated CG neurons from hypertensive rats. Moreover, the firing frequencies of tonic neurons were significantly lower in hypertensive rats compared to matched normotensive rats. Furthermore several K+ currents were found different in CG from the same animal model. Delay rectifier K+ current (IKv), big conductance Ca2+-activated K+ current (IBK) and A-type K+ current (IA) were significantly lower in hypertensive rats compared to normotensive rats. The contribution of the decreased K+ currents to neuronal firing changes in hypertension is confirmed by using specific K+ channel blockers. H2O2, one type of ROS, was applied to dissociated CG neurons. H2O2 caused more accommodating firing by converting tonic neurons to phasic/adaptive and adaptive neurons to phasic in response to sustained suprathreshold current injection. Neuronal firing frequency was also decreased by H2O2. All the changes in neuronal firing by H2O2 are similar to those differences between normotensive and hypertensive rats. Moreover H2O2 mimicked some of the reductions of K currents in hypertension by decreasing IA and IBK. In conclusion, the changes in distribution of different neuronal firing patterns, associated with attenuated K+ currents, are contributed by elevated ROS in CG neurons from hypertensive rats. The electrophysiological changes in CG might contribute to the increased sympathetic activity in DOCA-salt hypertensive rats.
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