Abstract
Effects of sematilide, a novel class III antiarrhythmic agent, on the delayed rectifier K+ current (IK) were examined in guinea pig atrial myocytes using a voltage clamp technique. Sematilide inhibited both time-dependent outward current upon depolarization and tail currents (IK-tail) at −40 mV. The concentration of sematilide required for a 50% decrease in IK-tail was approximately 50 μM. The sematilidesensitive current obtained using a triangular voltage command exhibited marked inward rectification and had the maximum amplitude at −30 mV. These results suggest that sematilide inhibits rapidly activating IK in guinea pig atrial myocytes, resulting in the prolongation of action potential duration and refractoriness.
