自发性高血压大鼠血管内皮功能不全发生机理实验研究

Study of mechanism on endothelial dysfunction of spontaneous hypertensive rats

目的探讨自发性高血压大鼠(SHR)血管内皮功能不全的发生机理。方法用SHR作为实验组,Wistar-Kyoto(WKY)大鼠作为正常对照组,采用尾动脉测压方法测定SHR和WKY大鼠血压;铜离子活化镉还原法测定血清中NO3-浓度;放射免疫分析法测定大鼠血或动脉组织中cGMP和内皮素(ET)水平。结果与WKY大鼠比较,SHR血中ET和NO3-水平均明显降低(P<0.01);动脉组织中cGMP含量亦明显降低(P<0.01),ET含量略增加但无显著性差异(P>0.05)。结论SHR体内一氧化氮的生成或释放不足可能直接参与血管内皮功能不全的发生,而ET水平可能不起主要作用。

ObjectiveTo investigate the mechanism on endothelial dysfunction of spontaneous hypertensive rats (SHR).MethodsThe animals were divided into two groups: SHRs (n=8) and Wistar-Kyoto (WKY) rats (n=7) all aged 17 months. Blood pressure was measured by the tail-cuff method. NO_3^- concentration in serum was assayed by activated cadmium reduction method; endothelin (ET) and cGMP levels were assayed by RIA.ResultsCompared with WKY rats, blood NO_3^- concentration, ET level and vascular cGMP level of SHRs were all reduced significantly ( P<0.01); vascular ET level was only uplifted slightly with no significant difference ( P>0.05).ConclusionIt indicates that the vascular endothelial dysfunction in SHR is induced possibly by a diminished synthesis or release of NO, not by changes of ET level.