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应用细胞内微电极和肌张力记录技术，观察了ET-1对豚鼠乳头肌细胞电生理和机械收缩活动的影响。结果表明：ET－1浓度依赖地明显延长PPD和APD90，增加心肌收缩张力；钾通道阻断剂TEA不影响ET-1的生物效应；而L型钙通道阻断剂硝苯吡啶、ETA受体选择性拮抗剂BQ-123和APⅢ以浓度依赖的方式阻断ET-1的上述效应，提示ET-1对乳头肌的电生理和正性肌力效应是由ETA受体亚型介导的，与胞浆内Ca2+升高有关。
The effects of ET-1 on the electrophysiological and mechanical contractile activity of guinea pig papillary muscle cells were observed by intracellular microelectrode and muscle tension recording technology. The results showed that: ET-1 significantly prolonged PPD and APD90 in a concentration-dependent manner and increased myocardial contractile tension; potassium channel blocker TEA did not affect the biological effects of ET-1; while L-type calcium channel blockers nifedipine and ETA receptor The selective antagonists BQ-123 and APIII blocked the above effects of ET-1 in a concentration-dependent manner, suggesting that electrophysiological and inotropic effects of ET-1 on papillary muscles are mediated by ETA receptor subtypes, Cytoplasmic Ca2 + increased.