双侧输尿管梗阻后大白鼠肾脏水通道蛋白2的变化

目的选择大白鼠模拟双侧输尿管梗阻模型,检测其肾脏水通道蛋白2(AQP2)的变化,以期从分子水平上阐明泌尿系梗阻解除后排尿量增多的病理生理改变。方法选取3个月雄性慕尼黑大白鼠(MunichWistarRats)12只,体重225g左右,随机分为实验组(n=6)及对照组(n=6),实验组行双侧输尿管梗阻24h后解除梗阻,对照组仅行输尿管游离而不结扎。每日观察体重、饮水量、食量、尿量变化,3d后取出肾标本,左肾全肾、右肾分离出内髓后行免疫杂交试验,检测水通道蛋白2(AQP2)的变化。结果解除输尿管梗阻后,实验组体重迅速下降(P<0.001),并排出大量低渗性尿液,渗透压明显低于对照组(P<0.05),术后每日排出尿量显著增高(P<0.001);血浆渗透压增高(312±4.71vs301±0.45mmol/L,P<0.05)。全肾及内髓检查,发现AQP2明显降低(P<0.01),而以集合管为主的内髓更为敏感。结论泌尿系梗阻影响肾脏对尿液的重吸收和浓缩功能,排出大量低渗尿液,同时体重明显下降,体内脱水严重;AQP2表达减少是肾脏集合管重吸收水分少、尿液浓缩功能差的主要原因。

The expression of renal Aquaporins2 in rats after the release of bilateral ureteral obstruction

Objective To examine whether release of BUO was associated with changes in the expression of renal AQP2, and whether such changes paralleled with changes in urinary output and urinary concentrating capacity in young rats.Methods Munich Wistar Rats were divided into two groups randomly (BUO n =6, Sham n =6) and kept in metabolic cages for measurements of urinary output, water and food intake, and body weight. Ureters were obstructed for 24?h and then released in BUO group. The sham group had their ureters freed but not ligated. Three days after the release, blood samples were collected from the aortas and the kidneys were removed to determine the expression levels of AQP2 by semi quantitative immunoblotting.Results Expressions of AQP2 in BUO group was lower than those in sham group both in the inner medulla and in the whole kidney.The release of BUO was also associated with immediate onset of predominant osmotic dependent polyuria ( P < 0.01 ), significant weight reduction ( P < 0.01 ), and plasma osmolality increase ( P < 0.05 ).Conclusions BUO decreases renal abilities for re absorption and concentration resulting in osmotic dependent polyuria.The down regulation of AQP2 may be the major contributing factor for that obstructive nephropathy.