Interaction between endothelin and angiotensin II in the up-regulation of vasopressin messenger RNA in the inner medullary collecting duct of the rat.
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.
Wang
Min Hui
MH
Department of Medicine, University of British Columbia, Vancouver Hospital and Health Sciences Center, Vancouver, British Columbia, Canada.
Fok
Alice
A
Huang
Min Ho
MH
Wong
Norman L M
NL
D000804:Angiotensin II / Q000494:pharmacology*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D015153:Blotting, Western; D065130:Endothelin A Receptor Antagonists; D065131:Endothelin B Receptor Antagonists; D016232:Endothelins / Q000494:pharmacology*; D007679:Kidney Medulla / Q000187:drug effects / Q000378:metabolism*; D007685:Kidney Tubules, Collecting / Q000187:drug effects / Q000378:metabolism*; D012333:RNA, Messenger / Q000096:biosynthesis* / Q000235:genetics; D051381:Rats; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012504:Saralasin / Q000494:pharmacology; D015854:Up-Regulation / Q000187:drug effects; D014667:Vasopressins / Q000096:biosynthesis* / Q000235:genetics*
D000806:Angiotensin-Converting Enzyme Inhibitors; D065130:Endothelin A Receptor Antagonists; D065131:Endothelin B Receptor Antagonists; D016232:Endothelins; D012333:RNA, Messenger; D014667:Vasopressins; D000804:Angiotensin II; D012504:Saralasin