{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,22]],"date-time":"2026-01-22T17:39:10Z","timestamp":1769103550984,"version":"3.49.0"},"reference-count":37,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2009,1,29]],"date-time":"2009-01-29T00:00:00Z","timestamp":1233187200000},"content-version":"vor","delay-in-days":1185,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2005,11]]},"abstract":"<jats:p>\n<jats:list list-type=\"explicit-label\">\n<jats:list-item><jats:p>The effectiveness of a selective endothelin receptor\u2010A (ET\u2010A) antagonist, A\u2010127722 (approximately 10\u2003mg\u2003kg<jats:sup>\u22121<\/jats:sup>\u2003day<jats:sup>\u22121<\/jats:sup> as 200\u2003mg\u2003kg<jats:sup>\u22121<\/jats:sup> powdered food), to reverse existing cardiac remodelling and prevent further remodelling was tested in deoxycorticosterone acetate (DOCA)\u2010salt hypertensive rats.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Uninephrectomised rats (UNX) administered DOCA (25\u2003mg every fourth day s.c.) and 1% NaCl in drinking water for 28 days developed hypertension (systolic blood pressure (BP): UNX 128\u00b16\u2003mmHg, DOCA\u2010salt 182\u00b15<jats:sup>*<\/jats:sup>\u2003mmHg; <jats:sup>*<\/jats:sup><jats:italic>P<\/jats:italic>&lt;0.05 vs UNX), left ventricular hypertrophy (UNX 1.99\u00b10.06\u2003mg\u2003kg<jats:sup>\u22121<\/jats:sup> body wt, DOCA\u2010salt 3.30\u00b10.08<jats:sup>*<\/jats:sup>\u2003mg\u2003kg<jats:sup>\u22121<\/jats:sup> body wt), decreased left ventricular internal diameter (UNX 6.69\u00b10.18\u2003mm, DOCA\u2010salt 5.51\u00b10.37<jats:sup>*<\/jats:sup>\u2003mm), an increased left ventricular monocyte\/macrophage infiltration together with an increased interstitial collagen from 2.7\u00b10.3 to 11.7\u00b11.3%, increased passive diastolic stiffness (UNX 21.1\u00b10.5, DOCA\u2010salt 30.1\u00b11.3<jats:sup>*<\/jats:sup>), prolongation of the action potential duration at 20 and 90% of repolarisation (APD<jats:sub>20<\/jats:sub>\u2013UNX 6.8\u00b11.1, DOCA\u2010salt 10.1\u00b11.5<jats:sup>*<\/jats:sup>\u2003ms; APD<jats:sub>90<\/jats:sub>\u2013UNX 34.4\u00b13.5\u2003ms, DOCA\u2010salt 64.3\u00b110.4<jats:sup>*<\/jats:sup>\u2003ms) and vascular dysfunctions (2.6\u2010fold decrease in maximal contractile response to noradrenaline, 3.5\u2010fold decrease in maximal relaxation response to acetylcholine).<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Administration of A\u2010127722 for 14 days starting 14 days after surgery attenuated the increases in systolic BP (150\u00b16<jats:sup>**<\/jats:sup>\u2003mmHg, <jats:sup>**<\/jats:sup><jats:italic>P<\/jats:italic>&lt;0.05 vs DOCA\u2010salt), left ventricular wet weight (2.65\u00b10.06<jats:sup>**<\/jats:sup>\u2003mg\u2003kg<jats:sup>\u22121<\/jats:sup> body wt) and internal diameter (6.39\u00b10.31<jats:sup>**<\/jats:sup>\u2003mm), prevented left ventricular monocyte\/macrophage accumulation, attenuated the increased left ventricular interstitial collagen (7.6\u00b11.3%<jats:sup>**<\/jats:sup>), reversed the increased passive diastolic stiffness (22.1\u00b11.2<jats:sup>**<\/jats:sup>), attenuated the action potential duration prolongation (APD<jats:sub>20<\/jats:sub> \u2013 7.6\u00b11.4<jats:sup>**<\/jats:sup>, APD<jats:sub>90<\/jats:sub> \u2013 41.5\u00b16.9<jats:sup>**<\/jats:sup>\u2003ms) and normalised changes in vascular function.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>ET\u2010A receptor antagonism both reverses and prevents the cardiac and vascular remodelling in DOCA\u2010salt hypertension and improves cardiovascular function.<\/jats:p><\/jats:list-item>\n<\/jats:list>\n<\/jats:p><jats:p><jats:italic>British Journal of Pharmacology<\/jats:italic> (2005) <jats:bold>146<\/jats:bold>, 846\u2013853. doi:<jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" xlink:href=\"10.1038\/sj.bjp.0706384\">10.1038\/sj.bjp.0706384<\/jats:ext-link><\/jats:p>","DOI":"10.1038\/sj.bjp.0706384","type":"journal-article","created":{"date-parts":[[2005,9,9]],"date-time":"2005-09-09T04:55:21Z","timestamp":1126241721000},"page":"846-853","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":27,"title":["Reversal of cardiac dysfunction by selective ET\u2010A receptor antagonism"],"prefix":"10.1111","volume":"146","author":[{"given":"Anthony","family":"Allan","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andrew","family":"Fenning","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Scott","family":"Levick","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andrew","family":"Hoey","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lindsay","family":"Brown","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2009,1,29]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.103.2.319"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1161\/hy0202.103481"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cardiores.2005.04.020"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.37.2.781"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.1007\/BF00167222"},{"key":"e_1_2_6_7_1","first-page":"S143","article-title":"Reversal of cardiac fibrosis in deoxycorticosterone acetate\u2010salt hypertensive rats by inhibition of the renin\u2013angiotensin system","volume":"10","author":"BROWN L.","year":"1999","journal-title":"J. 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