Parasympathetic effects on electrophysiologic properties of cardiac ventricular tissue.
The physiologic importance of parasympathetic influence on the sinoatrial and atrioventricular nodes is well established, but the importance of parasympathetic modulation of ventricular function remains controversial. Recognized effects of muscarinic cholinergic stimulation on ventricular automaticity and ventricular repolarization, the ability of muscarinic cholinergic agonists to antagonize catecholamine effects in the ventricle and proposed mechanisms for these effects are described. Anatomic studies have demonstrated a great abundance of cholinergic nerve endings in association with the ventricular conducting system. Stimulation of the vagus nerve or addition of muscarinic cholinergic agonists suppresses ventricular automaticity in most species and antagonizes isoproterenol-induced action potential shortening and isoproterenol-restored slow response action potentials. In vivo, interactions between the parasympathetic and sympathetic nervous systems occur at multiple levels. Muscarinic cholinergic agonists inhibit release of norepinephrine from sympathetic nerve terminals, inhibit catecholamine-stimulated adenylate cyclase activity and alter cyclic guanosine monophosphate (GMP) and possibly cyclic adenosine monophosphate (AMP) levels. Evidence is also presented that, in vivo, parasympathetic effects on ventricular electrical function might influence the pathophysiologic milieu responsible for initiation or termination of certain ventricular arrhythmias. Vagal influences appear to be protective against certain digitalis-induced arrhythmias and protective in certain experimental acute myocardial infarctions. In human beings, there appears to be tonic vagal tone in the ventricle and vagal stimulation terminates certain types of ventricular tachycardia. The evidence presented supports a physiologic role of parasympathetic stimulation in altering ventricular electrical function.
D000109:Acetylcholine / Q000494:pharmacology / Q000502:physiology*; D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000139:chemically induced / Q000503:physiopathology; D001285:Atropine / Q000494:pharmacology; D002395:Catecholamines / Q000037:antagonists & inhibitors / Q000494:pharmacology; D002415:Cats; D004071:Digitalis Glycosides / Q000494:pharmacology; D004285:Dogs; D004336:Drug Antagonism; D004562:Electrocardiography; D004594:Electrophysiology; D006801:Humans; D007545:Isoproterenol / Q000494:pharmacology; D009203:Myocardial Infarction / Q000503:physiopathology; D009638:Norepinephrine / Q000097:blood; D011690:Purkinje Fibers / Q000502:physiology; D011950:Receptors, Cholinergic / Q000502:physiology; D011976:Receptors, Muscarinic / Q000502:physiology; D014630:Vagus Nerve / Q000502:physiology; D016276:Ventricular Function
D002395:Catecholamines; D004071:Digitalis Glycosides; D011950:Receptors, Cholinergic; D011976:Receptors, Muscarinic; D001285:Atropine; D007545:Isoproterenol; D000109:Acetylcholine; D009638:Norepinephrine