Department of Pharmacology, Toho University Faculty of Pharmaceutical Sciences, Funabashi, Chiba 274-8510, Japan.
Biol Pharm Bull. 2010;33(1):138-41. doi: 10.1248/bpb.33.138.
Effects of NIP-142, a benzopyran compound which terminates experimental atrial arrhythmia, on potassium channel alpha-subunits and mouse atrial repolarization were examined. NIP-142 concentration-dependently blocked the outward current through potassium channel alpha subunits Kv1.5, Kv4.2 and Kv4.3 expressed in Xenopus oocytes. In isolated mouse atrial myocardia, NIP-142 prolonged the action potential duration and effective refractory period, and increased the contractile force. These results suggest that NIP-142 blocks the potassium channels underlying the transient and sustained outward currents, which may contribute to its antiarrhythmic activity.
研究了苯并吡喃化合物 NIP-142 对钾通道 alpha 亚基和小鼠心房复极的影响，该化合物可终止实验性心房性心律失常。NIP-142 浓度依赖性地阻断了在非洲爪蟾卵母细胞中表达的钾通道 alpha 亚基 Kv1.5、Kv4.2 和 Kv4.3 的外向电流。在分离的小鼠心房心肌中，NIP-142 延长了动作电位时程和有效不应期，并增加了收缩力。这些结果表明，NIP-142 阻断了瞬时和持续外向电流所依赖的钾通道，这可能有助于其抗心律失常活性。
