AJP - Heart and Circulatory Physiology, Vol 247, Issue 2 244-H250, Copyright © 1984 by American Physiological Society
Adrenergic-cholinergic interactions on membrane potential of K+ -depolarized ventricular muscle
T. Ehara and T. Mitsuiye
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.
