Why the study?
Does sematilide inhibit delayed rectifier K+ current in guinea pig atrial myocytes?
Does sematilide inhibit delayed rectifier K+ current in guinea pig atrial myocytes?
Sematilide acts as a class III antiarrhythmic by inhibiting the rapidly activating delayed rectifier K+ current (IKr) in atrial myocytes, which contributes to the prolongation of action potential duration and refractoriness.
Supports IKr inhibition by sematilide in guinea pig myocytes; leaves open clinical antiarrhythmic utility.
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 microM. The sematilide-sensitive 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.
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Ishii et al. (1996) studied this question.
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