Presynaptic inhibition of cardiac vagal postganglionic nerves by neuropeptide Y.
Stimulation of cardiac sympathetic nerves evokes prolonged non-adrenergic, non-cholinergic attenuation of the action of the vagus nerve on heart rate-an effect mimicked by, and proposed to be due to neuropeptide Y (NPY), a peptide released from sympathetic nerve terminals. In anaesthetised dogs, the effects on heart rate of the cholinomimetic bethanechol were unaltered by sympathetic stimulation or administration of NPY sufficient to cause prolonged inhibition of cardiac vagal action. In isolated guinea pig atria, during effective ganglion blockade, the effects on heart rate of the cholinomimetic methacholine were unaltered by exogenous NPY which inhibited cardiac slowing induced by stimulation of vagal nerve terminals. It is suggested that NPY released from sympathetic nerves inhibits cardiac vagal effectiveness by an action on postganglionic nerve terminals.
Potter
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School of Physiology and Pharmacology, University of New South Wales, Kensington, Sydney, Australia.
D000818:Animals; D004285:Dogs; D005724:Ganglia / Q000187:drug effects*; D006168:Guinea Pigs; D006325:Heart Atria; D006329:Heart Conduction System / Q000187:drug effects*; D066298:In Vitro Techniques; D009411:Nerve Endings / Q000187:drug effects; D009433:Neural Inhibition; D009478:Neuropeptide Y / Q000494:pharmacology*; D013569:Synapses / Q000187:drug effects*; D014630:Vagus Nerve / Q000187:drug effects*
D009478:Neuropeptide Y