Cardiac sympathetic-parasympathetic interactions.
The cardiac response to neural activity in one autonomic division depends on the level of activity in the other autonomic division. The extent of this peripheral interaction varies considerably with the cardiac effector tissue under consideration. In sinoatrial nodal tissue the effect of efferent sympathetic activity is progressively attenuated as the level of vagal activity is increased. A similar type of interaction prevails in the regulation of atrioventricular (AV) junctional pacemaker tissue. Surprisingly, however, an analogous peripheral interaction cannot be detected with regard to the autonomic neural control of AV conduction. Strong vagal activity alone has only a weak negative inotropic effect on the ventricular myocardium. However, in the presence of a substantial background of sympathetic activity, the same level of vagal activity exerts a prominent negative inotropic effect. The peripheral autonomic influence occurs at prejunctional and postjunctional levels. Prejunctionally, acetylcholine (ACh) released from vagal terminals interacts with muscarinic receptors on postganglionic sympathetic terminals to inhibit norepinephrine (NE) release. Postjunctionally, the response of a cardiac effector cell to a given concentration of NE in the biophase will diminish as the concentration of ACh in the biophase is raised.
D000818:Animals; D001283:Atrioventricular Node / Q000502:physiology; D001285:Atropine / Q000494:pharmacology; D004285:Dogs; D004558:Electric Stimulation; D006321:Heart / Q000294:innervation*; D006339:Heart Rate; D006801:Humans; D009200:Myocardial Contraction; D009638:Norepinephrine / Q000502:physiology; D013564:Sympathetic Nervous System / Q000502:physiology*; D014630:Vagus Nerve / Q000502:physiology*; D016276:Ventricular Function
D001285:Atropine; D009638:Norepinephrine