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机构地区:[1]河北医科大学基础医学研究所生理室,石家庄050017
出 处:《生理学报》1997年第2期146-152,共7页Acta Physiologica Sinica
基 金:国家自然科学基金!39200043
摘 要: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。Effects of endothelin on electrophysiological activity and contractility were examined in guinea pig papillary muscle using intracellular microelectrode and contractile tension recording technique. The results indicated that ET-1 prolonged APD, especially PPD and increased the contractile tension in a dose-dependent manner. The ET-induced effects were not influenced by K+ channel blocker TEA, but inhibited by L-type Ca2+channel blocker nifedipine, ETA receptor selective antagonist BQ-123 and atriopeptin Ⅲin a concentration-dependent manner. It is suggested that the changes in electrophysiological activity and the positive inotropic effect induced by ET-1 in guinea pig muscles are due to the elevation of intracellular calcium, which may be mediated by ETA receptor.
分 类 号:R337[医药卫生—人体生理学] Q516[医药卫生—基础医学]
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