自发性高血压大鼠主动脉血管功能的变化

Endothelial Dysfunction in Spontaneously Hypertensive Rats

目的 探讨自发性高血压大鼠 (SHR)血管舒缩功能变化及其可能机制。方法 以 32周龄SHR大鼠 (n =7)为研究对象 ,年龄、性别配对的WKY(n =7)大鼠作对照组。观察离体胸主动脉环对不同血管活性物质的舒缩反应。结果 SHR主动脉环对乙酰胆碱 (ACh)诱导的内皮依赖性舒张反应明显减弱 ;对ACh的内皮依赖性收缩反应明显高于WKY。L NAME加强ACh的收缩作用 ;对硝普钠 (SNP)的收缩反应在两组间无差别。结论 SHR大鼠存在内皮功能障碍 ,表现为内皮依赖性舒张作用减弱 ,其机制与内皮合成NO减少及内皮依赖性收缩作用增强有关。

Objective To compare the in vitro vasomotion function of the aorta in spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto (WKY) rats. Methods Vascular reactivity to vasoactive substances was studied with isolated rings of thoracic aorta from rats. Results Endothelium-dependent relaxation induced by ACh was significantly reduced in the SHR compared with the WKY control (49.54±9.18 vs 96.58±2.34, P <0.05). ACh also caused remarked endothelium-dependent contractile responses in SHR (SHR:5.37±0.73 vs WKY:0.53±0.16, P <0.01), which was augmented by inhibitors of NO-syntheses L-NAME(SHR:11.12±3.14 vs WKY:3.37±0.76, P <0.05). In contrast, there were no significant differences in the nitric oxide donor sodium nitroprusside (SNP) induced relaxations responses between SHR and WKY rats. Conclusion ACh-dependent relaxation is blunted in the SHR. Nitric oxide(NO) pathway plays an important role in the impairment of vasoactive function in SHR, while non-endothelium dependant relaxation seems not be attenuated.\ In SHR the vascular functional capacity of relaxation of respond to NO appear not to be altered.