Multiple roles for CNS GABA mechanisms in the autonomic regulation of cardiovascular function: Pharmacologic evidence

Abstract

Drugs which impair GABAergic inhibition by different mechanisms evoke similar cardiovascular changes. In the brainstem, these agents excite vagal preganglionic neurons, possibly by disrupting tonic inhibition at the nucleus ambiguus, and thus cause bradycardia. Acting in the periventricular forebrain, these same drugs suppress vagal activity while simultaneously enhancing sympathetic outflow. We propose that these actions represent impairment of two distinct GABAergic mechanisms impacting on cardiac vagal function, one controlling the final common pathway, the parasympathetic preganglionic neuron, the other inhibiting a latent system of hypothalamic “command neurons” whose activation results in cardiac vagal suppression as but one facet of a richer and highly integrated autonomic response.