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Twelve weeks after inducing <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content>, rats were treated with or without losartan (20\u00a0mg\/kg; daily) for 8\u00a0weeks and assessed for cardiac function, cardiac remodelling, subcellular alterations and plasma catecholamines. Cardiac hypertrophy and lung congestion in 20\u00a0weeks <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content>\u2010induced heart failure were associated with increases in plasma catecholamine levels. Haemodynamic examination revealed depressed cardiac function, whereas echocardiographic analysis showed impaired cardiac performance and marked increases in left ventricle wall thickness and chamber dilatation at 20\u00a0weeks of inducing <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content>. These changes in cardiac function, cardiac remodelling and plasma dopamine levels in heart failure were partially or fully reversed by losartan. Sarcoplasmic reticular (<jats:styled-content style=\"fixed-case\">SR<\/jats:styled-content>) <jats:styled-content style=\"fixed-case\"><jats:roman>Ca<\/jats:roman><\/jats:styled-content><jats:sup>2+<\/jats:sup>\u2010pump activity and protein expression, protein and gene expression for phospholamban, as well as myofibrillar (<jats:styled-content style=\"fixed-case\">MF<\/jats:styled-content>) <jats:styled-content style=\"fixed-case\"><jats:roman>Ca<\/jats:roman><\/jats:styled-content><jats:sup>2+<\/jats:sup>\u2010stimulated ATPase activity and \u03b1\u2010myosin heavy chain m<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> levels were depressed, whereas \u03b2\u2010myosin heavy chain expression was increased in failing hearts; these alterations were partially reversed by losartan. Although <jats:styled-content style=\"fixed-case\">SR <jats:roman>Ca<\/jats:roman><\/jats:styled-content><jats:sup>2+<\/jats:sup>\u2010release activity and m<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> levels for <jats:styled-content style=\"fixed-case\">SR <jats:roman>Ca<\/jats:roman><\/jats:styled-content><jats:sup>2+<\/jats:sup>\u2010pump were decreased in failing heart, these changes were not reversed upon losartan treatment; no changes in m<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> levels for <jats:styled-content style=\"fixed-case\">SR <jats:roman>Ca<\/jats:roman><\/jats:styled-content><jats:sup>2+<\/jats:sup>\u2010release channels were observed in untreated or treated heart failure. These results suggest that the partial improvement of cardiac performance in heart failure due to <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content> by losartan treatment is associated with partial reversal of cardiac remodelling as well as partial recovery of <jats:styled-content style=\"fixed-case\">SR<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">MF<\/jats:styled-content> functions.<\/jats:p>","DOI":"10.1111\/j.1582-4934.2012.01623.x","type":"journal-article","created":{"date-parts":[[2012,9,4]],"date-time":"2012-09-04T15:47:19Z","timestamp":1346773639000},"page":"2958-2967","source":"Crossref","is-referenced-by-count":11,"title":["Reversal of subcellular remodelling by losartan in heart failure due to myocardial infarction"],"prefix":"10.1111","volume":"16","author":[{"given":"Andrea","family":"Babick","sequence":"first","affiliation":[{"name":"Department of Physiology Institute of Cardiovascular Sciences St Boniface Hospital Research Winnipeg Manitoba Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Donald","family":"Chapman","sequence":"additional","affiliation":[{"name":"Department of Physiology Institute of Cardiovascular Sciences St Boniface Hospital Research Winnipeg Manitoba Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shelley","family":"Zieroth","sequence":"additional","affiliation":[{"name":"Division of Cardiology Faculty of Medicine University of Manitoba Winnipeg Manitoba Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Vijayan","family":"Elimban","sequence":"additional","affiliation":[{"name":"Department of Physiology Institute of Cardiovascular Sciences St Boniface Hospital Research Winnipeg Manitoba Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Naranjan S.","family":"Dhalla","sequence":"additional","affiliation":[{"name":"Department of Physiology Institute of Cardiovascular Sciences St Boniface Hospital Research Winnipeg Manitoba Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2012,12,13]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0735-1097(99)00630-0"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.carpath.2004.12.002"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1999.79.1.215"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.81.4.1161"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(97)00277-0"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1007\/s10741\u2010011\u20109278\u20107"},{"key":"e_1_2_7_8_1","doi-asserted-by":"publisher","DOI":"10.1006\/jmcc.1996.0353"},{"key":"e_1_2_7_9_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(98)00110-2"},{"key":"e_1_2_7_10_1","doi-asserted-by":"publisher","DOI":"10.2174\/0929867033457656"},{"key":"e_1_2_7_11_1","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/cvn281"},{"key":"e_1_2_7_12_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0828-282X(06)70315-4"},{"key":"e_1_2_7_13_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0895-7061(99)00103-X"},{"key":"e_1_2_7_14_1","first-page":"40","article-title":"Plasma norepinephrine, plasma\u2010renin activity, and congestive heart failure. 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