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To test the hypothesis that during Ang <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content> infusion, oxidative and nitrosative damage is mediated through both the mineralocorticoid receptor (<jats:styled-content style=\"fixed-case\">MR<\/jats:styled-content>) and angiotensin type 1 receptor (<jats:styled-content style=\"fixed-case\">AT<\/jats:styled-content>1), five groups of Sprague\u2013Dawley rats were studied: (i) control; (ii) Ang <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content> infused (80\u00a0ng\/min\u00a0\u00d7\u00a028\u00a0days); (iii) Ang <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\u00a0+\u00a0<jats:styled-content style=\"fixed-case\">AT<\/jats:styled-content>1 receptor blocker (<jats:styled-content style=\"fixed-case\">ARB<\/jats:styled-content>; 10\u00a0mg losartan\/kg per day\u00a0\u00d7\u00a021\u00a0days); (iv) Ang <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\u00a0+\u00a0mineralocorticoid receptor (<jats:styled-content style=\"fixed-case\">MR<\/jats:styled-content>) antagonist (Epl; 100\u00a0mg eplerenone\/day\u00a0\u00d7\u00a021\u00a0days); and (v) Ang <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\u00a0+\u00a0<jats:styled-content style=\"fixed-case\">ARB<\/jats:styled-content>\u00a0+\u00a0Epl (Combo;\u00a0\u00d7\u00a021\u00a0days). Both <jats:styled-content style=\"fixed-case\">ARB<\/jats:styled-content> and combination treatments completely alleviated the Ang <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\u2010induced hypertension, whereas eplerenone treatment only prolonged the onset of the hypertension. Eplerenone treatment exacerbated the Ang <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\u2010mediated increase in plasma and heart aldosterone 2.3\u2010 and 1.8\u2010fold, respectively, while <jats:styled-content style=\"fixed-case\">ARB<\/jats:styled-content> treatment reduced both. Chronic <jats:styled-content style=\"fixed-case\">MR<\/jats:styled-content> blockade was sufficient to ameliorate the <jats:styled-content style=\"fixed-case\">AT<\/jats:styled-content>1\u2010mediated increase in oxidative damage. All treatments normalized protein oxidation (nitrotyrosine) levels; however, only <jats:styled-content style=\"fixed-case\">ARB<\/jats:styled-content> and Combo treatments completely reduced lipid peroxidation (4\u2010hydroxynonenal) to control levels. Collectively, these data suggest that receptor signalling, and not the elevated arterial blood pressure, is the principal culprit in the oxidative stress\u2010associated cardiovascular damage in Ang <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\u2010dependent hypertension.<\/jats:p>","DOI":"10.1111\/1440-1681.12473","type":"journal-article","created":{"date-parts":[[2015,8,1]],"date-time":"2015-08-01T08:10:58Z","timestamp":1438416658000},"page":"1178-1188","source":"Crossref","is-referenced-by-count":17,"title":["Angiotensin and mineralocorticoid receptor antagonism attenuates cardiac oxidative stress in angiotensin <scp>II<\/scp>\u2010infused rats"],"prefix":"10.1111","volume":"42","author":[{"given":"Jacqueline N","family":"Minas","sequence":"first","affiliation":[{"name":"Molecular Cell Biology School of Natural Sciences University of California Merced CA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Max A","family":"Thorwald","sequence":"additional","affiliation":[{"name":"Molecular Cell Biology School of Natural Sciences University of California Merced CA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Debra","family":"Conte","sequence":"additional","affiliation":[{"name":"Molecular Cell Biology School of Natural Sciences University of California Merced CA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jose\u2010Pablo","family":"V\u00e1zquez\u2010Medina","sequence":"additional","affiliation":[{"name":"Molecular Cell Biology School of Natural Sciences University of California Merced CA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Akira","family":"Nishiyama","sequence":"additional","affiliation":[{"name":"Department of Pharmacology Kagawa Medical University Kagawa Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rudy M","family":"Ortiz","sequence":"additional","affiliation":[{"name":"Molecular Cell 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