Effect of NIP-142 on Potassium Channel .ALPHA.-Subunits Kv1.5, Kv4.2 and Kv4.3, and Mouse Atrial Repolarization

DOI Web Site 参考文献20件
  • Tanaka Hikaru
    Department of Pharmacology, Toho University Faculty of Pharmaceutical Sciences
  • Namekata Iyuki
    Department of Pharmacology, Toho University Faculty of Pharmaceutical Sciences
  • Hamaguchi Shogo
    Department of Pharmacology, Toho University Faculty of Pharmaceutical Sciences
  • Kawamura Taro
    Department of Pharmacology, Toho University Faculty of Pharmaceutical Sciences
  • Masuda Hiroyuki
    Department of Pharmacology, Toho University Faculty of Pharmaceutical Sciences
  • Tanaka Yoshio
    Department of Pharmacology, Toho University Faculty of Pharmaceutical Sciences Department of Chemical Pharmacology, Toho University Faculty of Pharmaceutical Sciences
  • Iida-Tanaka Naoko
    Department of Pharmacology, Toho University Faculty of Pharmaceutical Sciences Department of Food Science, Otsuma Woman's University
  • Takahara Akira
    Department of Pharmacology, Toho University Faculty of Pharmaceutical Sciences

抄録

Effects of NIP-142, a benzopyran compound which terminates experimental atrial arrhythmia, on potassium channel α-subunits and mouse atrial repolarization were examined. NIP-142 concentration-dependently blocked the outward current through potassium channel α 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.

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