{"title":"Renal effects of angiotensin II: role of prostaglandins?","authors":"J Shohat, A Erman, G Boner, J B Rosenfeld","doi":"10.1159/000173117","DOIUrl":null,"url":null,"abstract":"<p><p>In the present study the possible role of endogenous prostaglandins in modulating the renal effects of angiotensin II was investigated in the isolated perfused rat kidney. Angiotensin II (5 ng/ml) caused both an increase in prostaglandin E2 synthesis and an increase in renal vascular resistance, as well as an increase in perfusate flow rate and glomerular filtration rate. Filtration fraction did not change. Inhibition of prostaglandin synthesis did not influence these effects of angiotensin II. In addition, angiotensin II caused natriuresis and to a lesser degree kaliuresis. These effects were independent of intrarenal hemodynamic effects. Inhibition of renal prostaglandin synthesis did not have any effect on the angiotensin-induced natriuresis. We conclude that the natriuretic effect of angiotensin II is independent of renal prostaglandin synthesis.</p>","PeriodicalId":77779,"journal":{"name":"Renal physiology","volume":"10 2","pages":"85-92"},"PeriodicalIF":0.0000,"publicationDate":"1987-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000173117","citationCount":"4","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Renal physiology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1159/000173117","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 4
Abstract
In the present study the possible role of endogenous prostaglandins in modulating the renal effects of angiotensin II was investigated in the isolated perfused rat kidney. Angiotensin II (5 ng/ml) caused both an increase in prostaglandin E2 synthesis and an increase in renal vascular resistance, as well as an increase in perfusate flow rate and glomerular filtration rate. Filtration fraction did not change. Inhibition of prostaglandin synthesis did not influence these effects of angiotensin II. In addition, angiotensin II caused natriuresis and to a lesser degree kaliuresis. These effects were independent of intrarenal hemodynamic effects. Inhibition of renal prostaglandin synthesis did not have any effect on the angiotensin-induced natriuresis. We conclude that the natriuretic effect of angiotensin II is independent of renal prostaglandin synthesis.