中文摘要：

目的研究高血压大鼠胸主动脉以及周期性张应变刺激下血管平滑肌细胞（VSMCs）的Rho蛋白解离抑制因子（RhoGDIα）的表达变化,探讨血管紧张素Ⅱ（AngⅡ）信号通路对其表达的调控影响。方法应用实时PCR和Western blotting技术分别检测4周、12周和18周自发性高血压大鼠（SHR,n=4）和正常血压京都种鼠（WKY,n=4）胸主动脉RhoGDIαmRNA和蛋白的表达;免疫组织化学检测RhoGDIα在SHR和WKY胸主动脉的定位;Westernblotting技术检测腹主动脉缩窄性高血压大鼠（ACR,n=6）胸主动脉RhoGDIα蛋白的表达;应用细胞应变加载系统对大鼠胸主动脉VSMCs施加1Hz、10%的周期性张应变,在有或无血管紧张素亚型Ⅰ（AT1）受体拮抗剂L-158809的条件下观察周期性张应变刺激对VSMCs RhoGDIα蛋白表达的影响。结果4周与12周SHR和WKY胸主动脉RhoGDIα表达无显著性差异,而在18周组,SHR胸主动脉RhoGDIα表达显著高于WKY。RhoGDIα主要存在于血管中膜VSMCs。2周和4周ACR胸主动脉RhoGDIα表达较正常对照组显著上调,提示在高血压状...

英文摘要：

Objective To evaluate the role of angiotensin Ⅱ （Ang Ⅱ ） signal passway on the expression of Rho GDP dissociation inhibitor alpha （RhoGDIa） in hypertensive rats. Methods Protein and mRNA expressions of RhoGD1α in aortae of 4, 12 and 18 week-old spontaneously hypertensive rats （SHR, n = 4） and Wistar Kyoto rats （WKY, n = 4） were examined by Western blotting and real-time PCR. Aortas from SHR and WKY were analyzed using immonuchemical staining to locate the RhoGDIα in the aorta. The RhoGDla expression in aorta of hypertensive rat model of aorta coarctation （ACR, n = 6） was also analyzed using Western blotting. Furthermore, The effect of mechanical strain at 10 % elongation on expression of RhoGDIa in vascular smooth muscle cells （VSMCs） in the presence or absence of L-158809, an antagonist for Ang Ⅱ type 1 receptor, was also evaluated by Western blotting. Results No significant difference of RhoGDIa expression was found between SHR and WKY at 4- week-old and 12-week-old. However, in 18-week-old group, RhoGDIo was significantly highly expressed in SHR than that of WKY at both mRNA and protein levels. RhoGDIa was located in the media of the aorta. Expression of RhoGDIa protein was upregulated in aortas of ACR at 2 and 4 weeks as compared with the controls. The expression of RhoGDIa in VSMCs was inhibited by mechanical strain at 10 % elongation, and further decreased by treatment of L-158809. Conclusion RhoGDIa is upregulated in aortae of the hypertensive rats. AngⅡ signal passway may be involved in the process of regulating expression of RhoGDIa.