水钠潴留在痰湿壅盛证高血压大鼠模型中的机制研究

Mechanism of Water-Sodium Retention of Hypertensive Rats with Abundant Accumulation of Phlegm and Dampness Syndrome

目的:由饮食诱导建立高血压痰湿壅盛证大鼠模型,探讨水钠潴留在痰湿壅盛证高血压大鼠模型的机制。方法:由高脂饮食诱导建立高血压痰湿壅盛证大鼠模型,与普通Wistar大鼠对照,观察两组大鼠一般生理情况,应用酶联免疫法(ELISA)检测大鼠血清中的甘油三酯(TG)、胆固醇(TC)、超氧化物歧化酶(SOD)、血管加压素(AVP)及血管紧张素Ⅱ(AngⅡ)等变化,光镜观察肾组织和脂肪组织的形态结构,实时荧光定量PCR和蛋白质免疫印迹法(Western blot)检测肾脏ATlR、AT2R和AQP2的mRNA和蛋白的表达。结果:与正常对照组比较,模型组大鼠血中TG、TC、AVP、AngⅡ均明显升高(P<0.05),模型组大鼠肾脏AT1R、AQP2的mRNA和蛋白表达上调(P<0.05),AT2RmRNA和蛋白表达下降(P<0.05)。结论:饮食诱导高血压痰湿壅盛型大鼠肾脏存在水钠潴留的病理机制。

The study was aimed to investigate the mechanism of water-sodium retention of obesity-related hypertensive rats with abundant accumulation of phlegm and dampness syndrome.Obesity-related hypertensive rats with abundant accumulation of phlegm and dampness syndrome,which referred to the model group,were induced by high-fat diet.Levels of triglyceride（TG）,total cholesterol（TC）,superoxide dismutase（SOD）,vasopressin（AVP） and angiotensin Ⅱ（Ang Ⅱ） in serum were detected by the enzyme linked immunosorbent assays（ELISA）.The morphological structures of renal and adipose tissues were observed by light microscope.The mRNA and protein expressions of AT1 R,AT2R and AQP2 in kidney were examined by real-time polymerase chain reaction（PCR） and western blot.The results showed that compared with the normal control group,serum TG,TC,AVP and Ang Ⅱ in the model group increased significantly（P〈0.05）,and mRNA and protein expressions of AT1 R and AQP2 in kidney was up regulated（P〈0.05）.The mRNA and protein expressions of AT2 R were decreased（P〈0.05）.It was concluded that water and sodium retention took part in the kidney injury of obese hypertensive rats,which may be one of the important mechanisms in obesity-related hypertension.