{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T16:40:21Z","timestamp":1791909621103,"version":"4.3.4"},"reference-count":53,"publisher":"Portland Press Ltd.","issue":"9","content-domain":{"domain":["portlandpress.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2013,11,1]]},"abstract":"<jats:p>The aim of the present study was to investigate the coronary effects of Ang-(1\u20137) [angiotensin-(1\u20137)] in hypertrophic rat hearts. Heart hypertrophy was induced by abdominal aorta CoA (coarctation). Ang-(1\u20137) and AVE 0991, a non-peptide Mas-receptor agonist, at picomolar concentration, induced a significant vasodilation in hearts from sham-operated rats. These effects were blocked by the Mas receptor antagonist A-779. Pre-treatment with L-NAME (NG-nitro-L-arginine methyl ester) or ODQ (1H-[1,2,4]oxadiazolo[4,3-a]quinozalin-1-one) [NOS (NO synthase) and soluble guanylate cyclase inhibitors respectively] also abolished the effect of Ang-(1\u20137) in control hearts. The coronary vasodilation produced by Ang-(1\u20137) and AVE 0991 was completely blunted in hypertrophic hearts. Chronic oral administration of losartan in CoA rats restored the coronary vasodilation effect of Ang-(1\u20137). This effect was blocked by A-779 and AT2 receptor (angiotensin II type\u00a02 receptor) antagonist PD123319. Acute pre-incubation with losartan also restored the Ang-(1\u20137)-induced, but not BK (bradykinin)-induced, coronary vasodilation in hypertrophic hearts. This effect was inhibited by A-779, PD123319 and L-NAME. Chronic treatment with losartan did not change the protein expression of Mas and AT2 receptor and ACE (angiotensin-converting enzyme) and ACE2\u00a0in coronary arteries from CoA rats, but induced a slight increase in AT2 receptor in aorta of these animals. Ang-(1\u20137)-induced relaxation in aortas from sham-operated rats was absent in aortas from CoA rats. In\u00a0vitro pre-treatment with losartan restored the Ang-(1\u20137)-induced relaxation in aortic rings of CoA rats, which was blocked by the Mas antagonist A-779 and L-NAME. These data demonstrate that Mas is strongly involved in coronary vasodilation and that AT1 receptor (angiotensin II type\u00a01 receptor) blockade potentiates the vasodilatory effects of Ang-(1\u20137) in the coronary beds of pressure-overloaded rat hearts through NO-related AT2- and Mas-receptor-dependent mechanisms. These data suggest the association of Ang-(1\u20137) and AT1 receptor antagonists as a potential therapeutic avenue for coronary artery diseases.<\/jats:p>","DOI":"10.1042\/cs20120519","type":"journal-article","created":{"date-parts":[[2013,5,30]],"date-time":"2013-05-30T08:15:32Z","timestamp":1369901732000},"page":"449-459","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":48,"title":["Angiotensin II type\u00a01 receptor blockade restores angiotensin-(1\u20137)-induced coronary vasodilation in hypertrophic rat hearts"],"prefix":"10.1042","volume":"125","author":[{"given":"\u00c1lvaro\u00a0P. S.","family":"Souza","sequence":"first","affiliation":[{"name":"Department of Physiological Sciences, Federal University of Goi\u00e1s, Goi\u00e2nia 74001-970, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Deny\u00a0B. 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