【摘要】 目的研究血管紧张素Ⅱ受体-1阻断剂氯沙坦对肾性高血压大鼠血管重塑及其分裂原激活的蛋白激酶p38MAPK表达的影响。方法两肾一夹法复制肾血管性高血压大鼠(2K1C-RHR)模型;采用尾动脉套管法和颈动脉插管法测量大鼠血压,大血管(胸主动脉)苏木素-伊红(HE)染色进行形态学观察;治疗组采用氯沙坦灌胃治疗;反转录-聚合酶链反应和免疫印迹方法检测主动脉血管p38MAPK的表达。结果实验组大鼠和对照组(假手术组)普通饲料饲养6周,模型组血压为(158±7)mmHg,对照组血压为(104±11)mmHg;两组间差异有显著性(P<0.05);模型组大鼠胸主动脉内径增大,中层厚度增大,细胞层数略微增加。经氯沙坦治疗后,血压降为(132±9)mmHg,血管重塑现象氯沙坦治疗组较实验组明显改善;免疫印迹方法检测,重塑血管主动脉血管p38MAPK的表达增高,氯沙坦干预可以抑制其表达。结论氯沙坦可明显改善肾血管性高血压大鼠血管重塑,这种调节可能是通过阻断血管紧张素Ⅱ受体信号途径或调节p38MAPK表达而发挥作用。更多还原

【Abstract】 objective To investigate the effects of losartan,a specific blocker of angiotensinⅡ(AngⅡ)receptor(AT1),on vascular remodeling and p38MAPK expression in two-kidney,one-clip hypertensive rat.Methods The sys-temic blood pressure(SBP)was measured by tail-cuff method and carotid cannulation.The morphologic change of aor-tas was analyzed after HE staining.Western blot was per formed to detect p38MAPK expression.Result The SBP in hypertension group was significantly higher than that of control group(158±7mm Hg vs104±11mm Hg,P<0.05);treatment with losartan normalized SBP(132±9mm Hg).The ratio of lumen to media of mesenteric resistance arteries was decreased obviously in hypertension group;treatment with losartan improved vascular remodeling.The expression of p38MAPK increased in hypertension group,treatment with losartan could decrease the expression.Conclusion Losartan could prevent development of hypertension by regulating vascular remodeling in2KIC hypertensive rats,the mechanism is maybe to inhibit AngⅡsignal pathway or regulate expression of p38MAPK.更多还原