Noncompetitive catecholamine-antagonism of acetylcholine in the sympathectomized mammalian ventricular myocardium.
The effect of the vagus transmitter on the ventricular myocardium varies qualitatively as well as quantitatively in different warm-blood species. In the ventricular myocardium of birds (duck, hen), a part of the acetylcholine sensitivity remains even after catecholamine depletion. In contrast, the inhibitory effects of acetylcholine on the ventricular myocardium of mammals (rat, guinea pig, cat, dog, man) depend on the activity of the sympathicus. In the chemically sympathectomized (6-OH-DA) cat ventricular myocardium, a cholinergic innervation is, histochemically, clearly demonstrable. Correspondingly significant effects of endogenous (i.e. releasable by field stimulation) and exogenous acetylcholine can be seen if the contraction force is enhanced by exogenous catecholamines. This preparation is, therefore, a good model for the demonstration of a catecholamine antagonism of acetylcholine. Using this model, on the basis of dose-response relationships, it is possible to demonstrate that a noncompetitive catecholamine-antagonism of acetylcholine indeed exists in the mammalian ventricular myocardium independent of a cholinergically mediated reduction in the norepinephrine release.
D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D002395:Catecholamines / Q000037:antagonists & inhibitors*; D002415:Cats; D004285:Dogs; D006168:Guinea Pigs; D006321:Heart / Q000187:drug effects*; D006352:Heart Ventricles / Q000187:drug effects; D006801:Humans; D006892:Hydroxydopamines / Q000494:pharmacology; D009200:Myocardial Contraction / Q000187:drug effects; D051381:Rats; D013562:Sympathectomy
D002395:Catecholamines; D006892:Hydroxydopamines; D000109:Acetylcholine