Huang Y T, Hamilton C A, Reid J L
University Department of Materia Medica, Stobhill General Hospital, Glasgow, UK.
J Hypertens. 1989 Sep;7(9):703-5.
The ability of endothelin to stimulate phosphatidylinositol hydrolysis in rings of rat aorta was studied. Endothelin 10(-8)-10(-5) mol/l caused increases of 200-1000% in inositol phosphate levels. However, physiological responses to endothelin have been reported in the concentration range 10(-10)-10(-8) mol/l. Thus phosphatidylinositol hydrolysis as measured in the present study does not correlate directly with functional responses. Phosphatidylinositol hydrolysis in response to endothelin was attenuated but not abolished by removal of endothelium. Attenuation of inositol phosphate production was also observed with time, consistent with the hypothesis that continuous exposure to the agonist can cause desensitization of the endothelin receptor.
研究了内皮素刺激大鼠主动脉环中磷脂酰肌醇水解的能力。内皮素10(-8)-10(-5)mol/L可使肌醇磷酸水平升高200%-1000%。然而,据报道内皮素在10(-10)-10(-8)mol/L浓度范围内会产生生理反应。因此,本研究中所测定的磷脂酰肌醇水解与功能反应并不直接相关。去除内皮后,内皮素诱导的磷脂酰肌醇水解减弱但并未消除。随着时间的推移,还观察到肌醇磷酸生成的减弱,这与持续暴露于激动剂可导致内皮素受体脱敏的假说一致。