【摘要】 目的研究内皮素(ET)对离体Oddi括约肌收缩的直接影响,并对其传导通路进行探讨。方法(1)按累积加药法在K-H液中加入各浓度(0.1~100.0nmol/L)的ET-1,观察Oddi括约肌收缩频率及振幅的变化;(2)加入ET-1抗血清、尼卡地平、BQ-123后,再加入ET-1,测定三者对Oddi括约肌收缩的影响;检测Oddi括约肌PKC的活性。结果ET能收缩静息状态下的Oddi括约肌,其作用强度随ET浓度的增加而增强。随着ET-1浓度的增高,Oddi括约肌细胞胞浆蛋白激酶(PKC)活性也呈增高趋势。尼卡地平对ET所致的Oddi括约肌收缩反应无明显抑制作用,ET抗血清及BQ-123能显著抑制ET所致的Oddi括约肌的收缩。结论ET-1能明显收缩离体Oddi括约肌,其收缩强度与ET存在量效关系。ET抗血清和ET受体拮抗剂(BQ-123)对ET-1有较强的拮抗作用。PKC参与ET-1引起的Oddi约肌收缩的信号传导。更多还原

【Abstract】 Objective To investigate the direct effect of endothelin-1 on the contraction of Oddi sphincter,and study its signal transduction pathway.Methods By cumulative increase method,ET-1 was given in K-H solution up to the final concentration(0.1～100.0nmol/L),and the contraction amplitude and frequency of Oddi sphincter were observed.Anti-ET serum,nicardipine,and BQ-123 were added to detect their effects on the contraction of Oddi sphincter,and PKC activity in Oddi sphincter were also detected.Results ET addition resulted in the contraction of resting Oddis sphincter,and the contraction intensity increased with the rising ET concentration.No obvious inhibition effect on Oddis sphincter contraction was induced by nicardipine,while anti-ET serum and ET receptor antagonist reduced the Oddi sphincter contraction significantly.The PKC activity in cytoplasm of Oddi sphincter enhanced with the rising ET-1 concentration,and the contraction of Oddis sphincter increased at the same time.Conclusions ET-1 results in the significant contraction of the vivo Oddi sphincter,and the magnitude of contraction is dose-effect related to ET concentration.Anti-ET serum and ET receptor antagonists strongly offset the function of ET.PKC is involved in the signal transduction pathway of the Oddi sphincter contraction induced by ET-1.更多还原