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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Oddi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受体拮抗剂显著抑制了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受体拮抗剂对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。
Objective To study the direct effect of ET on contraction of isolated Oddi sphincter and to gain a preliminary understanding of its conduction pathways. Methods ET-1 in various concentration (0.1nM ~ 100nM) was added into KH solution by cumulative dosing method to observe the contraction frequency and amplitude of Oddi sphincter. ET-1 antiserum, Nicardipine and BQ-123 were added, -1, the determination of three of Oddi sphincter contraction; and detect Oddi sphincter PKC activity. Results ET attenuated the resting sphincter of Oddi, and the intensity of ET increased with the increase of ET concentration. Nicardipine had no significant inhibitory effect on the contractile response of Oddi sphincter induced by ET. ET antiserum and ET receptor antagonist significantly inhibited the contraction of Oddi sphincter. With the increase of ET-1 concentration, the cytoplasmic PKC activity of Oddi sphincter also increased, accompanied by the enhancement of Oddi sphincter contraction. Conclusions ET-1 can significantly constrict sphincter of Oddi in vitro, and there is dose-effect relationship between it and its contraction intensity. ET antiserum and ET receptor antagonist have a stronger antagonistic effect on ET-1. PKC is involved in the signaling of the contraction of the Oddi sphincter caused by ET-1.