{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,16]],"date-time":"2026-07-16T04:04:05Z","timestamp":1784174645722,"version":"3.55.0"},"reference-count":71,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2014,3,18]],"date-time":"2014-03-18T00:00:00Z","timestamp":1395100800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2014,3,18]],"date-time":"2014-03-18T00:00:00Z","timestamp":1395100800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2014,4]]},"abstract":"\n Background and Purpose<\/jats:title>\n \n The\n NO<\/jats:styled-content>\n redox sibling nitroxyl (\n HNO<\/jats:styled-content>\n ) elicits soluble guanylyl cyclase (\n sGC<\/jats:styled-content>\n )\u2010dependent vasodilatation.\n HNO<\/jats:styled-content>\n has high reactivity with thiols, which is attributed with\n HNO<\/jats:styled-content>\n \u2010enhanced left ventricular (\n LV<\/jats:styled-content>\n ) function. Here, we tested the hypothesis that the concomitant vasodilatation and inotropic actions induced by a\n HNO<\/jats:styled-content>\n donor,\n A<\/jats:styled-content>\n ngeli's salt (sodium trioxodinitrate), were\n sGC<\/jats:styled-content>\n \u2010dependent and\n sGC<\/jats:styled-content>\n \u2010independent respectively.\n <\/jats:p>\n <\/jats:sec>\n \n Experimental Approach<\/jats:title>\n \n Haemodynamic responses to\n A<\/jats:styled-content>\n ngeli's salt (10\u2009pmol\u201310\u2009\u03bcmol), alone and in the presence of scavengers of\n HNO<\/jats:styled-content>\n (\n L<\/jats:styled-content>\n \u2010cysteine, 4\u2009mM) or of\n NO<\/jats:styled-content>\n [hydroxocobalamin (\n HXC<\/jats:styled-content>\n ), 100\u2009\u03bcM] or a selective inhibitor of\n sGC<\/jats:styled-content>\n [1H\u2010[1,2,4]oxadiazolo[4,3\u2010a]quinoxalin\u20101\u2010one (\n ODQ<\/jats:styled-content>\n ), 10 \u03bcM], a\n CGRP<\/jats:styled-content>\n receptor antagonist (\n \n CGRP\n 8\u201337<\/jats:sub>\n <\/jats:styled-content>\n , 0.1\u2009\u03bcM) or a blocker of voltage\u2010dependent potassium channels [4\u2010aminopyridine (4\u2010\n AP<\/jats:styled-content>\n ), 1\u2009mM] were determined in isolated hearts from male rats.\n <\/jats:p>\n <\/jats:sec>\n \n Key Results<\/jats:title>\n \n A<\/jats:styled-content>\n ngeli's salt elicited concomitant, dose\u2010dependent increases in coronary flow and\n LV<\/jats:styled-content>\n systolic and diastolic function. Both\n L<\/jats:styled-content>\n \u2010cysteine and\n ODQ<\/jats:styled-content>\n shifted (but did not abolish) the dose\u2013response curve of each of these effects to the right, implying contributions from\n HNO<\/jats:styled-content>\n and\n sGC<\/jats:styled-content>\n in both the vasodilator and inotropic actions. In contrast, neither\n HXC<\/jats:styled-content>\n ,\n \n CGRP\n 8\u201337<\/jats:sub>\n <\/jats:styled-content>\n nor 4\u2010\n AP<\/jats:styled-content>\n affected these actions.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions and Implications<\/jats:title>\n \n Both vasodilator and inotropic actions of the\n HNO<\/jats:styled-content>\n donor\n A<\/jats:styled-content>\n ngeli's salt were mediated in part by\n sGC<\/jats:styled-content>\n \u2010dependent mechanisms, representing the first evidence that\n sGC<\/jats:styled-content>\n contributes to the inotropic and lusitropic action of\n HNO<\/jats:styled-content>\n in the intact heart. Thus,\n HNO<\/jats:styled-content>\n acutely enhances\n LV<\/jats:styled-content>\n contraction and relaxation, while concomitantly unloading the heart, potentially beneficial actions in failing hearts.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1111\/bph.12568","type":"journal-article","created":{"date-parts":[[2013,12,25]],"date-time":"2013-12-25T23:44:42Z","timestamp":1388015082000},"page":"1722-1734","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":24,"title":["The concomitant coronary vasodilator and positive inotropic actions of the nitroxyl donor\n A<\/scp>\n ngeli's salt in the intact rat heart: contribution of soluble guanylyl cyclase\u2010dependent and \u2010independent mechanisms"],"prefix":"10.1111","volume":"171","author":[{"given":"Kai Yee","family":"Chin","sequence":"first","affiliation":[{"name":"Heart Failure Pharmacology Baker IDI Heart & Diabetes Institute Melbourne Vic. Australia"},{"name":"School of Medical Sciences RMIT University Bundoora Vic. Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chengxue","family":"Qin","sequence":"additional","affiliation":[{"name":"Heart Failure Pharmacology Baker IDI Heart & Diabetes Institute Melbourne Vic. Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nga","family":"Cao","sequence":"additional","affiliation":[{"name":"Heart Failure Pharmacology Baker IDI Heart & Diabetes Institute Melbourne Vic. Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Barbara K","family":"Kemp\u2010Harper","sequence":"additional","affiliation":[{"name":"Department of Pharmacology Monash University Clayton Vic. Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Owen L","family":"Woodman","sequence":"additional","affiliation":[{"name":"School of Medical Sciences RMIT University Bundoora Vic. 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