The lack of currently available data stimulated us to investigate the electrophysiological effects of ajmaline, a classical class la antiarrhythmic agent, on various currents responsible for the action potential plateau and repolarization phases. The whole cell patch clamp recording technique was applied to guinea pig ventricular myocytes. Ajmaline suppressed the Ca2+ current (ICa) in a dose-dependent manner (Kd = 1.2 × 10-5 M) without affecting the steady-state inacti-vation kinetics and the voltage dependency of die current-voltage relationship. Ajmaline inhibited the inward portion of the inward rectifying K+ current (IKI). Ajmaline decreased the delayed rectifier K+ current (IK) without altering the activation or deactivation time courses. All these inhibitory effects of ajmaline prolonged the action potential duration in a dose dependent manner. The inhibitory actions of ajmaline on die action potential upstroke and various currents responsible for the plateau and repolarization may contribute to the observed suppression of depolarization-induced abnormal automaticities by this agent. (Jpn Heart J 36: 465-476, 1995).
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