correlations among plasma Ang II and ATI R and the film thick ness/diameter and membrane area/ cavity ( r = 0. 88 ~ 0. 93 ,P < 0. 01 ~ 0. 001) . And aorta Ang II level was closely related to the film thick ness/diameter and membrane area/cavity and expression of ATI R protein in VSMC of hypertension group ( r - 0. 82 ~ 0. 91 , P < 0. 01 ~ 0. 001). ?Compared with the operated group, SBP, MBP, LVMI and the membrane area/cavity area and the level of Ang II in aorta and the AT1R protein expressing of VSMC were significantly reduced in telmisartan group (P <0. 05). And aorta Ang II level and AT1R protein ex pressions of VSMC were significantly reduced in this group (P <0. 05). Conclusions Overexpression AT1R could contribute to vascular re modeling in experimental hypertensive rats. Telmisartan could reverse vascular remodeling by preventing the protein expression of AT1R in vessel.%目的 探讨替米沙坦对实验性高血压大鼠血管重构和AngⅡ1型受体(AT1R)的影响.方法 腹主动脉部分缩窄构建高血压大鼠模型,24只雌雄各半SD大鼠随机分成高血压组和替米沙坦组(3 mg·kg-1· d-1),另设假手术组为对照组.测定血流动力学指标和心室质量指数,主动脉进行图像分析,检测大鼠血浆与主动脉组织匀浆中血管紧张素Ⅱ(AngⅡ)含量,测定主动脉血管内皮细胞、血管平滑肌细胞AT1R蛋白的表达.结果 ①与假手术组比较,高血压组收缩压(SBP)、舒张压(DBP)、平均动脉压(MABP)、左室质量指数(LVMI)、中膜厚度/内径、中膜面积/内腔面积显著升高(P均<0.05);高血压组大鼠血浆与主动脉组织匀浆中AngⅡ含量和AT1R表达较对照组明显增高(P均<0.05);②高血压组血浆AngⅡ、血管平滑
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