两肾一夹型高血压大鼠重塑血管对血管紧张素II反应变化及其机制

The Change and the Mechanism in the Reactivity of Remodeling Vessel of Renal Hypertension Rats to Angiotensin Ⅱ

为了探讨两肾一夹型高血压大鼠重塑血管对血管紧张素Ⅱ的反应变化及其机制 ,在制作两肾一夹型高血压大鼠模型血管基础上 ,观察了两肾一夹型高血压大鼠大、小动脉的形态学改变 ;用肠系膜微血管口径显微电视测量法和离体血管环灌流实验分别观察了两肾一夹型高血压大鼠肠系膜动脉和胸主动脉对血管紧张素Ⅱ的反应以及洛沙坦对该反应的作用 ;并用逆转录 -聚合酶链反应检测两组动物胸主动脉血管紧张素Ⅱ 1型受体mRNA和 2型受体mRNA的表达。结果发现两肾一夹型高血压大鼠胸主动脉和肠系膜动脉中膜厚度增加 ,细胞层数增加 ,胶原纤维及弹力纤维含量增加 ;随着血管紧张素Ⅱ的浓度升高 ,肠系膜动脉、离体胸主动脉环收缩反应增加 ,而且在每一个血管紧张素Ⅱ浓度 ,两肾一夹型高血压大鼠肠系膜动脉和离体胸主动脉环对血管紧张素Ⅱ的收缩反应都比对照组增强 ;洛沙坦完全阻断离体胸主动脉环对血管紧张素Ⅱ的反应 ;两肾一夹型高血压大鼠胸主动脉血管紧张素Ⅱ 1型受体mRNA表达增多 ,血管紧张素Ⅱ 2型受体mRNA也有表达 ,而正常大鼠未见血管紧张素Ⅱ 2型受体mRNA表达。此结果提示 :(1)两肾一夹型高血压大鼠重塑血管对血管紧张素Ⅱ的反应增强 ,洛沙坦完全阻断血管对血管紧张素Ⅱ的反应 ;(2 )血管紧张素Ⅱ

Aim To investigate the mechanism of the change in the reactivity of the remodeling vessels of hypertension to Angiotensin Ⅱ(AngⅡ). Methods Use the method of Video-Microscope to observe the contractility of the third embranchment of the mesentery artery of the normotensive Sprague-Dawley (SD) rats and the two-kideny one-clip (2K1C) renal hypertension(RH) rats to AngⅡ. Use the method of isolation vascular ring perfusion to exploration the activity to AngⅡ of the aortic rings either group rats and the effect of losartan on the actibity. Use RT-PCR to measure AT1R mRNA and AT2R mRNA expression in the thoracic aorta of either group rats. Results All of the contractility of the aortic rings and the third embranchment of the mesentery artery to AngⅡ increased with dose-dependented, and the constractility of the remodeling vessels of the 2K1C RH rats to AngⅡ toned up more evidently at every dose of angiotensionⅡ. Loarstan block the the contractility of the aortic rings to AngⅡ completely. AT1R mRNA expression in the thoracic aorta of 2K1C RH rats is more than which in the the thoracic aorta of normotensive rats and AT2R mRNA express only in the thoracic aorta of 2K1C RH rats. Conclusions (1) The response of the remodeling vessel in hypertension to AngⅡtone up . (2) The mechanism of change in the reactivity of remodeling vessel of renal hypertension rats to Angiotensin Ⅱ may due to AT1R mRNA up-regulated.