Ishii Y, Muraki K, Kurihara A, Imaizumi Y, Watanabe M
Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, Nagoya City University, Japan.
Jpn J Pharmacol. 1996 Aug;71(4):361-5. doi: 10.1254/jjp.71.361.
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.
使用电压钳技术，在豚鼠心房肌细胞中研究了新型III类抗心律失常药物塞马利特对延迟整流钾电流（Ik）的影响。塞马利特抑制去极化时的时间依赖性外向电流以及 -40 mV 时的尾电流（Ik-tail）。使 Ik-tail 降低 50% 所需的塞马利特浓度约为 50 μM。使用三角电压指令获得的塞马利特敏感电流表现出明显的内向整流，并且在 -30 mV 时具有最大幅度。这些结果表明，塞马利特抑制豚鼠心房肌细胞中快速激活的 Ik，导致动作电位持续时间和不应期延长。
