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After the development of hypertension, rats were divided into four groups: 2K-1C (untreated), calcium channel blocker (amlodipine-treated), angiotensin receptor blocker (losartan-treated) and peripheral vasodilator (hydralazine-treated), which were treated for 10 weeks. Rats in the 2K-1C group had all developed hypertension, a significant increase in plasma levels of tumor necrosis factor alpha (TNF-\u03b1), interleukin 6 (IL-6), brain natriuretic peptide (BNP) and C-reactive protein (CRP). Moreover MA and creatininaemia underwent a significant increase. Under treatment decreases were observed in systolic blood pressure (SBP), TNF-\u03b1, CRP, IL-6, BNP concentrations and creatininaemia. These results were related to the absence of MA which was significantly associated with reductions in cardiac mass and hypertrophy markers (BNP and \u03b2-MHC gene expression) as well as renal interstitial inflammation. In conclusion, our results suggest that the reduction of MA is correlated with the decrease of the inflammatory components and seems to play an important role in protecting against cardiac hypertrophy and renal injury.<\/jats:p>","DOI":"10.33549\/physiolres.932146","type":"journal-article","created":{"date-parts":[[2020,3,28]],"date-time":"2020-03-28T07:49:45Z","timestamp":1585381785000},"page":"13-24","source":"Crossref","is-referenced-by-count":18,"title":["Cardiorenal Syndrome in Hypertensive Rats: Microalbuminuria, Inflammation and Ventricular Hypertrophy"],"prefix":"10.33549","author":[{"given":"M.","family":"MOUBARAK","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"H.","family":"JABBOUR","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"V.","family":"SMAYRA","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"E.","family":"CHOUERY","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Y.","family":"SALIBA","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"V.","family":"JEBARA","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"N.","family":"FAR\u00c8S","sequence":"additional","affiliation":[{"name":"Laboratoire de Physiologie et Physiopathologie, Facult\u00e9 de M\u00e9decine, Universit\u00e9 Saint Joseph, Beyrouth, Liban"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"19169","published-online":{"date-parts":[[2012,2,14]]},"reference":[{"key":"ref0","doi-asserted-by":"publisher","unstructured":"ARNLOV J, EVANS JC, MEIGS JB, WANG TJ, FOX CS, LEVY D, BENJAMIN EJ, D'AGOSTINO RB, VASAN RS: Low-grade albuminuria and incidence of cardiovascular disease events in nonhypertensive and nondiabetic individuals: the Framingham Heart Study. 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