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内皮素与血管紧张素II在大鼠髓质内集合管中血管加压素信使核糖核酸上调过程中的相互作用

Interaction between endothelin and angiotensin II in the up-regulation of vasopressin messenger RNA in the inner medullary collecting duct of the rat.

作者信息

Wang Min Hui, Fok Alice, Huang Min Ho, Wong Norman L M

机构信息

Department of Medicine, University of British Columbia, Vancouver Hospital and Health Sciences Center, Vancouver, British Columbia, Canada.

出版信息

Metabolism. 2007 Oct;56(10):1372-6. doi: 10.1016/j.metabol.2007.05.006.

Abstract

Recent studies in our laboratory have demonstrated that angiotensin (ANG) II and endothelin (ET) 1 up-regulate the expression of arginine vasopressin V(2) receptor in the inner medullary collecting duct (IMCD) of the rat. The present studies were performed to explore the interaction between ANG II and ET-1 in up-regulating the expression of arginine vasopressin V(2) receptor in the IMCD of the rat. Two sets of studies were done. In the first set of studies, rat IMCD tissue was isolated and incubated with ANG II in combination with ET(A) or ET(B) antagonist. In the second set of experiments, rat IMCD tissue was incubated with ET-1 with ANG receptor antagonist saralasin. Tissue samples were then analyzed by means of quantitative reverse transcriptase polymerase chain reaction and Western blotting. The ANG II treatment resulted in increased V(2) messenger RNA (mRNA) from control level of 138 +/- 12 amol/microg of total RNA to 385 +/- 63 amol/microg of total RNA (P < .01). The ANG II/ET(A) treatment resulted in no significant decrease in V(2) mRNA expression (319 +/- 59 amol/microg of total RNA), whereas ET-1/ET(B) antagonist and ET-1/ET(A)/ET(B) antagonist treatments resulted in reducing V(2) mRNA to control levels of 214 +/- 25 and 176 +/- 22 amol/microg of total RNA, respectively. The ET-1 treatment increased V(2) mRNA expression from control level of 221 +/- 25 amol/microg of total RNA to 383 +/- 43 amol/microg of total RNA (P < .02). The ET-1-induced increase in V(2) mRNA expression was significantly reduced to control level (210 +/- 36 amol/microg of total RNA) after saralasin treatment. Western blotting revealed that changes in protein expression in the different treatment conditions were comparable with changes in V(2) mRNA expression. These data suggested that the up-regulation of V(2) receptor induced by ANG II and ET-1 is mediated by both vasoconstricting hormones. These 2 systems interact in up-regulating the expression of V(2) receptors in the kidney.

摘要

我们实验室最近的研究表明,血管紧张素(ANG)II和内皮素(ET)1可上调大鼠髓质内层集合管(IMCD)中精氨酸加压素V2受体的表达。本研究旨在探讨ANG II与ET-1在大鼠IMCD中上调精氨酸加压素V2受体表达过程中的相互作用。进行了两组研究。在第一组研究中,分离大鼠IMCD组织,并将其与ANG II联合ET(A)或ET(B)拮抗剂一起孵育。在第二组实验中,将大鼠IMCD组织与ET-1及ANG受体拮抗剂沙拉新一起孵育。然后通过定量逆转录聚合酶链反应和蛋白质印迹法对组织样本进行分析。ANG II处理使V2信使核糖核酸(mRNA)从对照水平的每微克总RNA 138±12 amol增加至每微克总RNA 385±63 amol(P<.01)。ANG II/ET(A)处理导致V2 mRNA表达无显著下降(每微克总RNA 319±59 amol),而ET-1/ET(B)拮抗剂及ET-1/ET(A)/ET(B)拮抗剂处理分别使V2 mRNA降至对照水平的每微克总RNA 214±25 amol和176±22 amol。ET-1处理使V2 mRNA表达从对照水平的每微克总RNA 221±25 amol增加至每微克总RNA 383±43 amol(P<.02)。沙拉新处理后,ET-1诱导的V2 mRNA表达增加显著降至对照水平(每微克总RNA 210±36 amol)。蛋白质印迹法显示,不同处理条件下蛋白质表达的变化与V2 mRNA表达的变化相当。这些数据表明,ANG II和ET-1诱导的V2受体上调是由两种血管收缩激素介导的。这两个系统在肾脏中上调V2受体表达过程中相互作用。

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