{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T01:55:53Z","timestamp":1777859753449,"version":"3.51.4"},"reference-count":26,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[2008,9,1]],"date-time":"2008-09-01T00:00:00Z","timestamp":1220227200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Renin Angiotensin Aldosterone Syst"],"published-print":{"date-parts":[[2008,9]]},"abstract":"<jats:p>Introduction. Aldosterone promotes renal fibrosis via the mineralocorticoid receptor (MR), thus contributing to hypertension-induced nephropathy. We investigated whether MR gene expression influences renal fibrosis and MR antagonist response in a two-kidney, one-clip hypertensive rat model.<\/jats:p>\n                  <jats:p>Materials and methods. Brown Norway (BN), Lewis, and ACI rats were randomised to spironolactone 20 mg\/kg\/day or water by gavage, starting four weeks after left renal artery clipping. Blood pressure was measured bi-weekly by tail cuff. After eight weeks of treatment, right kidneys were removed and examined for fibrosis and gene expression. Rats of each strain undergoing no intervention served as controls.<\/jats:p>\n                  <jats:p>Results. Blood pressure increased similarly among strains after clipping and was unaffected by spironolactone. Hypertension caused the greatest renal fibrosis in BN rats (p &lt; 0.001 by ANOVA compared to other strains). Real-time PCR analysis showed greater renal collagen type I and MR gene expression in untreated, hypertensive BN rats (both p &lt; 0.05 compared to other strains). Spironolactone attenuated fibrosis, with similar fibrosis among strains of spironolactone-treated rats.<\/jats:p>\n                  <jats:p>Conclusion. Hypertension-induced renal fibrosis was greatest in rats with the highest MR gene expression. Spironolactone abolished inter-strain differences in fibrosis. Our data suggest that MR genotype may influence aldosterone-induced renal damage, and consequently, renal response to aldosterone antagonism.<\/jats:p>","DOI":"10.1177\/1470320308096367","type":"journal-article","created":{"date-parts":[[2008,10,20]],"date-time":"2008-10-20T11:35:16Z","timestamp":1224502516000},"page":"146-153","source":"Crossref","is-referenced-by-count":7,"title":["Hypertension-induced renal fibrosis and spironolactone response vary by rat strain and mineralocorticoid receptor gene expression"],"prefix":"10.1177","volume":"9","author":[{"given":"Larisa H.","family":"Cavallari","sequence":"first","affiliation":[{"name":"Department of Pharmacy Practice, College of Pharmacy, University of Illinois at Chicago, Chicago, IL 60612, USA,"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lucy A.","family":"Fashingbauer","sequence":"additional","affiliation":[{"name":"Department of Pharmacy Practice, College of Pharmacy, University of Illinois at Chicago, Chicago, IL 60612, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joseph R.","family":"Camp","sequence":"additional","affiliation":[{"name":"Department of Pharmacy Practice, College of Pharmacy, University of Illinois at Chicago, Chicago, IL 60612, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Stephen T.","family":"King","sequence":"additional","affiliation":[{"name":"Research Resources Center, University of Illinois at Chicago, Chicago, IL 60612, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David L.","family":"Geenen","sequence":"additional","affiliation":[{"name":"Department of Medicine, Section of Cardiology and Center for Cardiovascular Research, University of Illinois at Chicago, Chicago, IL 60612, 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