{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,15]],"date-time":"2026-05-15T04:09:29Z","timestamp":1778818169498,"version":"3.51.4"},"reference-count":30,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2006,7,18]]},"abstract":"<jats:p>\n            <jats:bold>\n              <jats:italic>Background\u2014<\/jats:italic>\n            <\/jats:bold>\n            Activation of the renin-angiotensin system (RAS) may contribute to the development of alcoholic cardiomyopathy. We evaluated the effect of angiotensin II (Ang II) type 1 receptor (AT\n            <jats:sub>1<\/jats:sub>\n            ) blockade on the development of alcoholic cardiomyopathy.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>Methods and Results\u2014<\/jats:italic>\n            <\/jats:bold>\n            We serially evaluated left ventricular (LV) and cardiomyocyte function and the RAS over 6 months in 3 groups of instrumented dogs. Eight animals received alcohol (once per day orally, providing 33% of total daily caloric intake); 6 received alcohol and irbesartan (5 mg \u00b7 kg\n            <jats:sup>\u22121<\/jats:sup>\n            \u00b7 d\n            <jats:sup>\u22121<\/jats:sup>\n            PO); and 8 were controls. Compared with controls, alcohol ingestion caused sustained RAS activation with progressive increases in plasma levels of Ang II, renin activity, LV angiotensin-converting enzyme activity, and LV myocyte Ang II AT\n            <jats:sub>1<\/jats:sub>\n            receptor expression. The RAS activation was followed by a progressive fall in LV contractility (E\n            <jats:sub>ES<\/jats:sub>\n            , alcohol-fed dogs 3.9\u00b10.8 versus control dogs 8.1\u00b11.0 mm Hg\/mL); reductions in the peak velocity of myocyte shortening (78.9\u00b15.1 versus 153.9\u00b16.2 \u03bcm\/s) and relengthening; and decreased peak systolic Ca\n            <jats:sup>2+<\/jats:sup>\n            transient ([Ca\n            <jats:sup>2+<\/jats:sup>\n            ]\n            <jats:sub>iT<\/jats:sub>\n            ) and L-type Ca\n            <jats:sup>2+<\/jats:sup>\n            current (\n            <jats:italic>I<\/jats:italic>\n            <jats:sub>Ca,L<\/jats:sub>\n            ;\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05). Irbesartan prevented the alcohol-induced decreases in LV and myocyte contraction, relaxation, peak [Ca\n            <jats:sup>2+<\/jats:sup>\n            ]\n            <jats:sub>iT<\/jats:sub>\n            , and\n            <jats:italic>I<\/jats:italic>\n            <jats:sub>Ca,L<\/jats:sub>\n            . With alcohol plus irbesartan, plasma Ang II, cardiac angiotensin-converting enzyme activity, and AT\n            <jats:sub>1<\/jats:sub>\n            remained close to control values.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>Conclusions\u2014<\/jats:italic>\n            <\/jats:bold>\n            Chronic alcohol consumption produces RAS activation followed by progressive cardiac dysfunction. The cardiac dysfunction is prevented by AT\n            <jats:sub>1<\/jats:sub>\n            receptor blockade.\n          <\/jats:p>","DOI":"10.1161\/circulationaha.105.596494","type":"journal-article","created":{"date-parts":[[2006,7,11]],"date-time":"2006-07-11T00:33:59Z","timestamp":1152578039000},"page":"226-236","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":73,"title":["Angiotensin II Type 1 Receptor Blockade Prevents Alcoholic Cardiomyopathy"],"prefix":"10.1161","volume":"114","author":[{"given":"Che-Ping","family":"Cheng","sequence":"first","affiliation":[{"name":"From the Cardiology Section, Department of Internal Medicine (C.-P.C., H.-J.C., D.C.S., T.W., W.C.L.), Department of Biochemistry (C.C.), and Department of Pathology (Z.K.S.), Wake Forest University School of Medicine, Winston-Salem, NC."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Heng-Jie","family":"Cheng","sequence":"additional","affiliation":[{"name":"From the Cardiology Section, Department of Internal Medicine (C.-P.C., H.-J.C., D.C.S., T.W., W.C.L.), Department of Biochemistry (C.C.), and Department of Pathology (Z.K.S.), Wake Forest University School of Medicine, Winston-Salem, NC."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Carol","family":"Cunningham","sequence":"additional","affiliation":[{"name":"From the Cardiology Section, Department of Internal Medicine (C.-P.C., H.-J.C., D.C.S., T.W., W.C.L.), Department of Biochemistry (C.C.), and Department of Pathology (Z.K.S.), Wake Forest University School of Medicine, Winston-Salem, NC."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zakariya K.","family":"Shihabi","sequence":"additional","affiliation":[{"name":"From the Cardiology Section, Department of Internal Medicine (C.-P.C., H.-J.C., D.C.S., T.W., W.C.L.), Department of Biochemistry (C.C.), and Department of Pathology (Z.K.S.), Wake Forest University School of Medicine, Winston-Salem, NC."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David C.","family":"Sane","sequence":"additional","affiliation":[{"name":"From the Cardiology Section, Department of Internal Medicine (C.-P.C., H.-J.C., D.C.S., T.W., W.C.L.), Department of Biochemistry (C.C.), and Department of Pathology (Z.K.S.), Wake Forest University School of Medicine, Winston-Salem, NC."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Thomas","family":"Wannenburg","sequence":"additional","affiliation":[{"name":"From the Cardiology Section, Department of Internal Medicine (C.-P.C., H.-J.C., D.C.S., T.W., W.C.L.), Department of Biochemistry (C.C.), and Department of Pathology (Z.K.S.), Wake Forest University School of Medicine, Winston-Salem, NC."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"William C.","family":"Little","sequence":"additional","affiliation":[{"name":"From the Cardiology Section, Department of Internal Medicine (C.-P.C., H.-J.C., D.C.S., T.W., W.C.L.), Department of Biochemistry (C.C.), and Department of Pathology (Z.K.S.), Wake Forest University School of Medicine, Winston-Salem, NC."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1378\/chest.121.5.1638"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2005.02.075"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1161\/res.88.3.298"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1161\/res.78.5.880"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.2001.280.4.H1853"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/0091-3057(86)90416-8"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1530-0277.1992.tb01368.x"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1530-0277.2001.tb02235.x"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1016\/0741-8329(86)90053-4"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.01045.2003"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0735-1097(98)00695-0"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.96.7.2385"},{"key":"e_1_3_2_13_2","unstructured":"Baughman KL. 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