Effects of nifedipine on electrical activity of cardiac cells

Abstract

The effects of nifedipine were studied on action potentials recorded from (1) normal canine Purkinje fibers, (2) Purkinje fibers exposed to barium chloride (0.1 to 0.25 m M), which reduces their membrane potential and produces enhanced pacemaker activity (abnormal automaticity), and (3) subendocardial Purkinje fibers underlying infarct zones at 24 hours after ligation of the left anterior descending coronary artery. In concentrations of 0.1 to 0.3 mg/liter, nifedipine did not significantly alter the resting transmembrane potential, action potential amplitude or maximal upstroke velocity of normal Purkinje fibers. The action potential duration (to 50 and 100 percent repolarization) was significantly shortened. These concentrations of nifedipine did not suppress the slope of phase 4 depolarization of automaticity in Purkinje fibers with maximal diastolic potentials between −85 and −95 mV. Abnormal automaticity in fibers exposed to barium chloride (Ba ++), having maximal diastolic potentials of −40 and −60 mV, was promptly abolished by nifedipine in concentrations of 20 to 200 μg/liter (n = 12). In slightly higher concentrations (0.2 to 0.6 mg/liter), nifedipine slowed or stopped abnormal automaticity in infarct zone Purkinje fibers (n = 3). In two subendocardial Purkinje fiber preparations, salvos of spontaneous impulses were observed that were terminated with delayed afterdepolarizations; nifedipine (0.1 to 0.2 mg/liter) quickly abolished these impulses. It is concluded that nifedipine can suppress abnormal automatic activity in canine cardiac Purkinje fibers in concentrations of 20 to 200 μg/liter, concentrations that will only shorten the plateau of normal action potentials. Nifedipine may prove to be a useful antiarrhythmic drug.