血管紧张素Ⅱ输注对肾小管管周毛细血管密度和肾小管缺氧的影响  

Effect of angiotensin Ⅱ infusion on density of peritubular capillary and hypoxia of kidney tubules

作　　者：牛伟静[1] 胡凤琪[1] 任志龙[1] 丁国华[1] 

机构地区：[1]武汉大学人民医院肾内科,430060

出　　处：《临床肾脏病杂志》2011年第8期367-369,共3页Journal Of Clinical Nephrology

基　　金：国家自然科学基金资助项目（30871167、81070556）

摘　　要：目的观察血管紧张素Ⅱ（AngⅡ）对低氧诱导因子1α（HIF．1α）表达及肾小管管周毛细血管（P1rC）密度的影响，探讨AngⅡ在肾小管损伤中的作用机制。方法将18只雄性SD大鼠随机分为3组，每组各6只。A组给予AngⅡ（400ng·k^-1·min^-1）持续输注28d；B组在A组基础上加用替米沙坦（3mg·kg^-1·d^-1）；C组为对照组，由生理盐水代替AngⅡ。每周末测量尾动脉收缩压、24h尿蛋白定量，于第28天处死动物。心脏采血后，测血肌酐（SCr），计算内生肌酐清除率（Ccr）；留取肾组织，免疫组织化学法检测肾组织CD31和HIF-1α分布及表达。结果A组血压和尿蛋白较C组高（P〈0．01），B组血压和尿蛋白较A组低（P〈0．05）。各组Ccr差异无统计学意义（P〉0．05）。A组P1、C密度较C组低（P〈0．05），B组较A组高（PG0．05）。A组HIF-1α表达较C组高（P〈0．05），B组较A组低（P〈0．01）。结论缺氧可能是AngⅡ引起肾小管损伤的机制之一。Objective To evaluate the effect of angiotensin Ⅱ （Ang H ） infusion on the expres- sion of the hypoxia-inducible factor 1α （HIF-1α） and the density of peritubu1αr capil1αry （PTC）. Methods Male Sprague Dawley rats were randomly divided into 3 groups （n = 6 each） ： group A （Ang Ⅱ was infused by 400 ng.kg^-1 .min^-1 for 28 days） ; group B （Telmisartan treatment at a dose of 3 mg. kg^-1.d^-1 on the basis of group A）; group C （0. 9% saline solution was used）. The systolic blood pressure was measured and the 24-h urine sample was collected for detection of proteinuria at every weekend. Animals were sacrificed at the day 28. Serum creatinine was determined in cardiac blood. The expression and location of HIF-1α and PTC were evaluated by immunohistochemical staining. Results Systolic blood pressure and proteinuria in group A were increased as compared with group C （P 〈0. 01）. Systolic blood pressure and proteinuria in group B were decreased as compared with group A （P〈0. 05）. Clearance rate of endogenous creatinine had no significant difference among three groups （P〈0. 05）. The PTC density was lower in group A than in group C （P〈0. 05）. The PTC density in group B was greater than in group A （P〈0. 05）. The expression of HIF-1α in group A was increased significantly as compared with group C（P〈0. 05）. The expression of HIF-1α in group B was de creased significantly as compared with group A （P〈0. 01）. Conclusions Hypoxia may be an important mechanism in Ang Ⅱ-induced damage of kidney tubules.

关 键 词：血管紧张素Ⅱ 低氧诱导因子1Α 毛细血管 

分 类 号：R322.81[医药卫生—人体解剖和组织胚胎学]