血管紧张素Ⅱ在肝硬化肾钠潴留中的作用  

Role of angiotensin Ⅱ on the renal sodium retention in cirrhosis

作　　者：申振宇[1] 蒋晓峰[2] 陶春华[1] 施嫣红[1] 郭传勇[1] 

机构地区：[1]同济大学附属第十人民医院消化内科,上海200072 [2]同济大学附属同济医院肾内科,上海200065

出　　处：《同济大学学报（医学版）》2008年第1期62-64,共3页Journal of Tongji University(Medical Science)

摘　　要：目的应用血管紧张素拮抗剂缬沙坦探讨血管紧张素Ⅱ在肝硬化肾钠潴留中的作用。方法64例肝硬化患者随机分为观察组和对照组,分别给予口服缬沙坦(80 mg/d)一周和常规治疗。用药前后分别测定血浆肾素活性(plasma renin activity,PRA)、血浆血管紧张素Ⅱ(angiotensinⅡ,AⅡ)及24 h尿钠(urinary sodium excretion per 24h,UNa+)。结果用药后PRA、AⅡ升高,同时UNa+排出增加,有腹水和肝损严重者尤为明显。结论缬沙坦使尿钠排出增加,表明AⅡ在肝硬化肾钠异常代谢中起重要作用。Objective Using valsartan, angiotensin receptor antagonist, to assess the role of angiotensin Ⅱ in renal sodium retention in cirrhosis. Methods Sixty-four patients with cirrhosis were divided into two groups as follows： 32 patients who received valsartan 80 mg/day for 7 days were of observation group and 32 patients who received routin treatment were of control group. Plasma renin activity（PRA）, plasma angiotensin Ⅱ level （AⅡ） and urinary sodium excretion per 24 h（UNa^＋ ）were measured before and after treatments. Results PRA,AⅡ and UNa^＋ were increased significantly after valsartan treatments especially in patients with ascites and greater severity of liver function. Conclusion That valsartan can increase the elimination of UNa^＋ suggests that A Ⅱ play an important and direct role on renal sodium retention in cirrhosis.

关 键 词：血管紧张素拮抗剂 缬沙坦 肝硬化 肾钠潴留 

分 类 号：R571[医药卫生—消化系统]