心力衰竭大鼠肾脏血管紧张素Ⅱ受体各亚型表达的改变

摘要

目的:探讨大鼠心力衰竭(心衰)时肾脏血管紧张素Ⅱ受体(angiotensin Ⅱ receptor ATR)各亚型表达水平的变化.方法:选择雄性Wistar大鼠35只,随机分为对照组(10只)、假手术组(10只)、其余15只制作心肌梗死后心衰模型成功9只为模型组.取大鼠肾脏皮质,采用反转录聚合酶链反应(RT-PCR)法分别测定各组大鼠ATR各亚型mRNA表达水平.结果:假手术组与对照组AT1R、AT2R比较,差异无统计学意义(P＞0.05);与假手术组比较,模型组大鼠AT1R表达明显上调,差异有统计学意义(P＜0.05),模型组大鼠AT2R表达明显下调,差异有统计学意义(P＜0.01).结论:心衰时肾脏AT1R明显上调,可能与此时RAS激活、血管紧张素Ⅱ(Ang Ⅱ)生成增多有关;而AT2R明显下调,提示肾脏代偿能力不足,最终会导致心衰肾脏的功能明显减退.%Objective:To explore the changes of expression of renal angiotensin Ⅱ receptor (ATR)subtypes in rats with heart failure. Metbods: Thirty-five male Wistar rats were randomly divided into three groups : control group( n = 10) , sham operation group( n = 10 ) , heart failure model group ( n = 9 , heart failure model was established successfully in 9 of 15 male Wistar rats). The mRNA levels of ATR subtypes of renal cortex were measured by reverse Uanscription polymerase Chain reaction ( RT-PCR) in each group. Results :Compared with control group , expression of AT1R and AT2R showed no difference in sham operation group ( P ＞0.05) , compared with sham operation group, expression of AT1R was increased significantly in heart failure model group(P ＜ 0.05 ) , expression of AT2R was decreased significantly in heart failure model group ( P ＜0.01 ) . Conclusion : The upregulation of renal AT1R may be associated with the activation of rennin-angiotensin system and the increased production of angiotensin Ⅱ. The downregulation of renal AT2R implied that the ability of renal compensation was insufficient, and then lead to the significant decrease of renal function in heart failure.