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pubmed:abstractText |
In guinea pig ventricular muscles exposed to K+-rich (27 mM) Tyrode solution containing 0.2 mM Ba, catecholamine elicited a slight depolarization of the resting membrane. Application of acetylcholine (ACh) during this catecholamine-induced response caused a repolarization, and removal of ACh induced a transient enhancement in the depolarization (rebound). These effects of ACh were abolished by atropine. Application of ACh alone and its removal had little effect on the membrane potential. Like the catecholamine-induced depolarization, the rebound depolarization after ACh removal was inhibited by slow channel blockers. Thus the rebound was attributed at least in part to enhanced changes in the catecholamine-sensitive conductance, i.e., a beta-receptor-mediated increase in the slow channel conductance. In driven muscles perfused with normal Tyrode solution, there was a rebound increase in twitch tension when ACh was removed in the presence of catecholamine, and this rebound was accompanied by an "extra" elevation of the action potential plateau. Thus cessation of the stimulation of myocardial muscarinic receptors may transiently lead to an enhanced activity of the beta-adrenoceptor-slow channel system in guinea pig ventricular muscle.
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