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.
出处
《生理学报》
CAS
CSCD
北大核心
1997年第2期146-152,共7页
Acta Physiologica Sinica
基金
国家自然科学基金!39200043
关键词
内皮素
乳头肌
电生理
肌肉收缩
endothelin
BQ-123
TEA
nifedipine
atriopeptinⅢ
pepillary muscle
electrophysiology
