Function of myocardial α-adrenoceptors

Abstract

Myocardial α-adrenoceptors are similar to vascular α-adrenoceptors; therefore the drugs which are used to study myocardial α-adrenoceptors can affect the heart indirectly by acting on vascular α-adrenoceptors. High concentrations of α-adrenoceptor stimulant and α-adrenoceptor blocking drugs can exert cardiac effects that do not result from action on α-adrenoceptors; therefore relatively low concentrations of these drugs must be used to obtain specific effects. An α-adrenoceptor mediated positive inotropic effect has been observed in relatively slow beating isolated heart preparations; it is not associated with shortening of the duration of systole or an increase in myocardial cyclic AMP concentration and is probably accompanied by an increase in Ca 2+ influx. Usually α-adrenoceptor stimulation has no effect on heart rate. Myocardial α-adrenoceptor mediated ventricular arrhythmias have been caused in animals by high concentrations of catecholamines, and a transient increase in α-adrenoceptor concentration has been found in ischemic myocardium. We do not know how myocardial α-adrenoceptor stimulation causes arrhythmias. In isolated heart preparations low concentrations of epinephrine and norepinephrine prolong refractory period and action potential duration by α-adrenoceptor stimulation, and higher concentrations of the catecholamines shorten refractory period and action potential duration by α-adrenoceptor stimulation. In isolated specialized conducting fibers low concentrations of catecholamines reduce automaticity by α-adrenoceptor stimulation and higher concentrations increase automaticity by β-adrenoceptor stimulation. In partially depolorized ventricle preparations α-adrenoceptor stimulation has been reported both to depress and to restore electrical and mechanical activity. Clearly, much remains to be done before we understand α-adrenoceptor mediated cardiac effects.