Effects of alpha-adrenergic agents on generation of oscillatory afterpotentials and triggered activity in rabbit Purkinje fibers

Abstract

Effects of α 1- and α 2-adrenergic agonists and antagonists on oscillatory afterpotentials (OAP) and triggered activity induced by acetylstrophanthidin (AS) or 8 m m Ca 2+ (with 2 m m K +) were studied with standard microelectrode techniques in isolated rabbit heart Purkinje fibers. Experiments were conducted in the presence of 0.5 μ m propranolol. Phenylephrine (PE, 0.5 to 10 μ m) increased the amplitude of OAP and induced triggered activity when subthreshold OAP were caused by high Ca 2+. In contrast, PE decreased the amplitude of OAP and suppressed triggered activity induced by acetylstrophanthidin. Prazosin at 0.5 μ m did not affect the amplitudes of OAP by itself, but abolished both the inhibitory effect of PE on AS-induced OAP and the stimulatory effect of PE on high Ca 2+-induced OAP. At 2 μ m, prazosin alone reduced the amplitude of OAP and suppressed triggered activity induced by either acetylstrophanthidin or high Ca 2+. While clonidine (0.5 to 10 μ m) did not affect OAP or induction of triggered activity, yohimbine (2 μ m) decreased the amplitude of OAP and abolished triggered activity induced by either acetylstrophanthidin or high Ca 2+. Thus, specific α 1-adrenergic actions of phenylephrine may exert either pro-arrhythmic or antiarrhythmic effects on OAP and triggered activity depending on the method of induction of OAP. The α 1- and α 2-antagonists prazosin and yohimbine both exert direct antiarrhythmic effects in addition to their adrenergic blocking actions.