Modulation of the intracardiac neurons of the guinea pig cardiac plexus by norepinephrine and Angiotensin II

Regulation of the guinea pig cardiac plexus by sympathetic neurotransmiiters and the renin‐angtiotensin system was examined in whole mounts using intracellular voltage recordings. Norepinephrine (NE) was applied to individual neurons and changes in both passive and evoked responses were determined. NE induced changes in the resting membrane potential, an inhibition of the action potential afterhyperpolarization, and an increase in neuronal excitability. The increase in NE‐induced excitability was unaffected by either 1 mM Ba 2+ or 1 mM Cs + , but was reduced with removal of extracellular Ca 2+ or addition of 200 μM Cd 2+ , indicating a dependence on extracellular calcium influx. The NE responses could be mimicked in most cells by either alpha 1 agonists or beta 2 agonists. Addition of angiotensin II (Ang II) to the bath solution resulted in a small increase in neuronal excitability and a significant potentiation of the norepinephrine‐induced increase in excitability. Addition of an AT 1 inhibitor to the bath solution had no effect on Ang II responses. However, addition of an AT 2 agonist to the bath mimicked the Ang II responses. These results indicate that the activity of parasympathetic postganglionic neurons can be differentially enhanced by alpha 1 or beta 2 adrenoreceptors and that response is potentiated by angiotensin II via AT 2 receptors. Supported by NIH HL098589 to JCH and EMS and HL71830 JLA.