Termination of Aconitine-Induced Atrial Fibrillation by the K<sub>ACh</sub>-Channel Blocker Tertiapin: Underlying Electrophysiological Mechanism

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  • Suzuki Kazumasa
    Department of Pharmacology, Chiba University Graduate School of Medicine, Japan
  • Matsumoto Akio
    Department of Pharmacology, Chiba University Graduate School of Medicine, Japan
  • Nishida Hirofumi
    Department of Pharmacology, Chiba University Graduate School of Medicine, Japan
  • Reien Yoshie
    Department of Pharmacology, Chiba University Graduate School of Medicine, Japan
  • Maruyama Hiroo
    Department of Pharmacology, Chiba University Graduate School of Medicine, Japan
  • Nakaya Haruaki
    Department of Pharmacology, Chiba University Graduate School of Medicine, Japan

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Other Title
  • Termination of Aconitine-Induced Atrial Fibrillation by the K[AC]h-Channel Blocker Tertiapin : Underlying Electrophysiological Mechanism
  • Termination of aconitine-induced atrial fibrillation by KACh-channel blocker tertiapin: underlying electrophysiological mechanism

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Abstract

The acetylcholine receptor–operated K+ (KACh) channel may be a novel target for atrial-specific antiarrhythmic therapy. Recently it has been demonstrated that tertiapin, a selective blocker of KACh channel, suppressed aconitine-induced atrial fibrillation (AF) in dogs. However, the precise mechanism by which the KACh-channel blocker inhibits the aconitine-induced AF remains unknown. This study was undertaken to determine the role of KACh channel in aconitine-induced AF in guinea pigs. Tertiapin terminated the aconitine-induced AF in anesthetized guinea pigs. The results of an in vitro electrophysiological experiment using atrial cells and atrial preparations suggest that aconitine might activate KACh channels in atrial cells, probably by intracellular Na+ accumulation, and inhibition of KACh channels by tertiapin might suppress AF by producing conduction block, probably due to further decrease in the resting membrane potential. Since it has been reported that constitutively active KACh channels can be observed in atrial cells of patients with chronic AF, aconitine-induced AF may be used as an experimental model for evaluation of drug effect on chronic AF.

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