{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T03:31:52Z","timestamp":1773459112987,"version":"3.50.1"},"reference-count":31,"publisher":"Canadian Science Publishing","issue":"6","license":[{"start":{"date-parts":[[2008,6,1]],"date-time":"2008-06-01T00:00:00Z","timestamp":1212278400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.nrcresearchpress.com\/page\/about\/CorporateTextAndDataMining"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Can. J. Physiol. Pharmacol."],"published-print":{"date-parts":[[2008,6]]},"abstract":"<jats:p> Renal collecting duct (CD)-specific knockout of endothelin-1 (ET-1) causes hypertension and impaired Na excretion. A previous study noted failure to suppress the renin\u2013angiotensin\u2013aldosterone axis in these knockout (KO) mice, hence the current investigation was undertaken to examine the role of this system in CD\u00a0ET-1\u00a0KO. Renal renin content was similar in kidneys from CD\u00a0ET-1\u00a0KO and control mice during normal Na intake; high-Na intake suppressed renal renin content to a similar degree in KO and control. Plasma renin concentrations paralleled changes in renal renin content. Valsartan, an angiotensin receptor blocker (ARB), abolished the hypertension in CD\u00a0ET-1\u00a0KO mice during normal Na intake. High-Na intake\u00a0+ ARB treatment increased blood pressure in CD\u00a0ET-1\u00a0KO, but not in controls. High-Na intake was associated with reduced Na excretion in CD\u00a0ET-1\u00a0KO animals, but no changes in water excretion or creatinine clearance were noted. Spironolactone, an aldosterone antagonist, also normalized blood pressure in CD\u00a0ET-1\u00a0KO mice during normal Na intake, whereas high-Na intake\u00a0+ spironolactone raised blood pressure only in CD\u00a0ET-1\u00a0KO animals. In summary, hypertension in CD ET-1 KO is partly due to angiotensin II and aldosterone. We speculate that CD-derived ET-1 may regulate, via a novel pathway, renal renin production. <\/jats:p>","DOI":"10.1139\/y08-028","type":"journal-article","created":{"date-parts":[[2008,5,30]],"date-time":"2008-05-30T19:06:48Z","timestamp":1212174408000},"page":"329-336","source":"Crossref","is-referenced-by-count":19,"title":["Role of the renin\u2013angiotensin\u2013aldosterone system in collecting duct-derived endothelin-1 regulation of blood pressureThis article is one of a selection of papers published in the special issue (part 1 of 2) on Forefronts in Endothelin."],"prefix":"10.1139","volume":"86","author":[{"given":"Yuqiang","family":"Ge","sequence":"first","affiliation":[{"name":"Division of Nephrology, University of Utah Health Sciences Center, 1900 East 30 North, Salt Lake City, UT 84132, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yufeng","family":"Huang","sequence":"additional","affiliation":[{"name":"Division of Nephrology, University of Utah Health Sciences Center, 1900 East 30 North, Salt Lake City, UT 84132, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Donald E.","family":"Kohan","sequence":"additional","affiliation":[{"name":"Division of Nephrology, University of Utah Health Sciences Center, 1900 East 30 North, Salt Lake City, UT 84132, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"155","reference":[{"key":"atypb1\/ref1","doi-asserted-by":"crossref","first-page":"S135","DOI":"10.1097\/00005344-199506263-00042","volume":"26","author":"Ackermann M.","year":"1995","journal-title":"J. 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