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目的：探讨内皮素-1在豚鼠乳头肌诱发异常电活动的特征及其离子机制。方法：用常规微电极技术引导并记录心肌细胞内电活动，分析其各参数。结果：ET-1浓度依赖地延长乳头肌细胞的APD，并在低Mg2+灌流的条件下诱发EADs。ET-1所诱发EADs的幅度、触发发放时程TBD具有明显的浓度依赖性和刺激周长依赖性。ETA受体拮抗剂BQ-123和Ca2+通道阻断剂硝苯吡啶可消除ET-1的上述作用。结论：ET-1通过ETA受体激活Ca2+通道，导致细胞内Ca2+超载进而诱发EADs。由于EADs的出现，致使心肌细胞复极化异常，可能是ET-1致心律失常作用的电生理基础“,”Objective: Present study focuses on the electrophysiologieal properties of arrhythunogenic action of endothelin and itsunderlying mechanisms. Methods: Transmembrane action potential (AP) in guinea pig papillary muscles were recorded withmicroelectrode and the parmeters of APs were analysed with computer. Results: ET1 significantly prolonged APD in concen-tration-dependent manner and induced stable EADs at lower concentration of [ Mg2 + ]0. The occurence of EADs induced by ET1, their amplitudes and triggered burst duration (TBD) were markdly dependent on the dose and the drive cycle length. Boththe prolongation APD and occurence of EADs evoked by ET-1 were abolished by either BQ-123,an ETA receptor selective antagonist,or Nif, a Ca2+ channel blocker. Conelusion: EADs induced by ET-1 in the papillary muscles might be attributed tointracellular Ca2+ overloading as result of an activation of Ca2+ channel via ETA receptor. ET-iduced abnormalities of reploarization, as were manifested by EADs, provided an important electrophysiological basis for the occurence of fatal arrhythmia.