内皮素对Oddi括约肌功能影响的实验研究

目的研究ET对离体Oddi括约肌收缩的直接影响，并对其传导通路进行初步的了解。方法按累积加药法在K-H液中加入各浓度（0．1nM-100nM）的ET-1，观察Oddi括约肌收缩频率及振幅的变化；加入ET-1抗血清、Nicardipine、BQ-123，再加入ET-1，测定三者对Od出括约肌收缩的影响；并检测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。Nicardipine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ET受体桔抗剂显著抑制了Oddi括约肌的收缩。随着ET-1浓度增高，Oddi括约肌细胞胞浆PKC活性也呈增高趋势，并伴随有Oddi括约肌收缩的增强。结论ET-1能明显收缩离体Oddi括约肌，且与其收缩强度存在量效关系。ET抗血清与ET受体桔抗剂对ET-1有较强的拮抗作用。PKC参与了ET-1引起的Oddi括约肌收缩的信号传导。

Study on the effect of endothelin-1 on the contraction of Oddi sphincter

[Objective] To investigate the direct effect of endothelin-1 on the contraction of Oddi sphincter, the signal transduction pathway was also explored. [Methods] Accumulated ET-1 were given in K-H solution to made a final concentration (0.1nM～100nM), the contraction amplitude and frequency of Oddi sphincter were observed,Anti-ET serum, Nicardipine, BQ-123 were added to detect their effects on the contraction of Oddi sphincter, and PKC activities in Oddi sphincter were also detected. [Results] ET addition resulted in the contraction of resting Oddi sphincter, and the contraction intensity increased with the rising ET concentration. No obvious inhibition effect on Oddi 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 Oddi sphincter increased at the same time. [Conclusion] ET-1 addition results in the significant contraction of the ex vivo Oddi sphincter, the contraction and ET concentration are dose-effect related. 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.