| 大鼠双侧输尿管梗阻后肾脏钠通道的改变 |
| |
| 引用本文： | 王贵宪,文建国.大鼠双侧输尿管梗阻后肾脏钠通道的改变[J].郑州大学学报(医学版),2004,39(6):947-950. |
| |
| 作者姓名： | 王贵宪 文建国 |
| |
| 作者单位： | 郑州大学第一附属医院尿动力学中心,郑州大学第一附属医院小儿外科,河南省高等学校临床医学重点学科开放实验室,郑州,450052;郑州大学第一附属医院尿动力学中心,郑州大学第一附属医院小儿外科,河南省高等学校临床医学重点学科开放实验室,郑州,450052 |
| |
| 基金项目： | 河南省杰出青年科学基金资助项目 0 2 12 0 0 0 110 0，河南省杰出人才创新基金资助项目 0 2 2 10 0 2 0 0 0，河南省高等学校创新人才培养工程项目2 0 0 2 -2 0 0 7 |
| |
| 摘 要： | 目的 :探讨泌尿系梗阻后肾脏功能的改变机制。方法 :2 0只大鼠随机分为实验组 (n =10 )及对照组 (n =10 )。实验组双侧输尿管梗阻 2 4h后解除梗阻 ,对照组手术同实验组 ,但不结扎。所有大鼠于术前 3d及术后 4d测量饮水量、食量、体重及尿量 ;术后 4d抽取动脉血化验 ,同时取出双侧肾脏 ;右肾全肾快速放入液氮冰冻备份 ,左肾分离出内髓 (IM)、外髓内带 (ISOM)、外髓外带加肾皮质 (OSOM +C) ,免疫杂交法检测 3型钠氢交换通道 (NHE3)、钠钾ATP酶 (Na -K -ATPase)和钠 -钾 - 2氯协同转运通道蛋白 (BSC - 1)。结果 :实验组输尿管梗阻 2 4h后引起肾脏水钠排泄异常 ,机体水电解质紊乱 ;肾脏不同部位NHE3、Na-K -ATPase及BSC - 1表达均较对照组降低 (P均<0 .0 1)。结论 :NHE3、Na-K -ATPase及BSC - 1水平降低可能是泌尿系梗阻后肾小管性钠回吸收障碍、低渗性尿量增多的主要原因之一
|
| 关 键 词： | 双侧输尿管梗阻 3型钠氢交换通道 钠钾ATP酶 钠-钾-2氯协同转运通道蛋白 大鼠 |
| 修稿时间： | 2004年9月28日 |
Expressions of major renal Na+ transporter in rats with bilateral ureteral obstruction |
| |
| WANG Guixian,WEN Jianguo Urodynamic Center.Expressions of major renal Na+ transporter in rats with bilateral ureteral obstruction[J].Journal of Zhengzhou University: Med Sci,2004,39(6):947-950. |
| |
| Authors: | WANG Guixian WEN Jianguo Urodynamic Center |
| |
| Institution: | WANG Guixian,WEN Jianguo Urodynamic Center,Department of Pediatric Surgery,the First Affiliated Hospital,the Open Key Clinical Medical Experimental Laboratory Institute of Universities of Henan Province,Zhengzhou University,Zhengzhou 450052 |
| |
| Abstract: | Aim: To explore the molecular mechanism of renal function defects after urinary obstruction. Methods: A total of 20 male Munich-Wister rats were randomly divided into bilateral ureteral obstruction (BUO) group and sham operated control (sham) group with 10 in each group. With the semiquantitative immunoboltting methods, the expression levels of type 3 Na +/H + exchanger (NHE3) ,Na-K-ATPase and type 1 bumetanide sensitive Na-K-2Cl cotransporter (BSC-1) were examined. The functional data were observed.Results: Consistent with polyuria and reduced urinary osmolality, the expressions of NHE3, Na-K-ATPase and BSC-1 of BUO group were lower than those of sham group. Conclusion: The downregulation of major renal sodium transporters after BUO may contribute to the impaired renal tubular sodium reabsorption, decreased urinary concentration, and postobstructive polyuria. |
| |
| Keywords: | bilateral ureteral obstruction type 3 Na +/H + exchanger Na-K-ATPase type 1 bumetanide sensitive Na-K-2Cl cotransporter rat |
| 本文献已被 CNKI 万方数据 等数据库收录！ |
|
