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Article: Inhibition of catecholamine-induced cardiac fibrosis by an aldosterone antagonist

TitleInhibition of catecholamine-induced cardiac fibrosis by an aldosterone antagonist
Authors
Issue Date2005
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/
Citation
Journal Of Cardiovascular Pharmacology, 2005, v. 45 n. 1, p. 8-13 How to Cite?
AbstractIn heart failure, the renin-angiotensin-aldosterone and the sympathetic systems are overactivated and lead to formation of cardiac fibrosis, which contributes to the aggravation of cardiac function. The aim of the present study was to evaluate the role of aldosterone and angiotensin II on formation of left ventricular fibrosis induced by chronic β-adrenergic stimulation with isoproterenol (iso) in the rat heart failure model induced by myocardial infarction (MI). Rats were submitted to chronic treatment with either the aldosterone receptor antagonist potassium canrenoate (pc, 20 mg/kg/d) or both aldosterone and angiotensin II receptor antagonists with addition of losartan (los, 10 mg/kg/d). Isoproterenol induced cardiac hypertrophy, which was completely inhibited by potassium canrenoate alone in atria and by potassium canrenoate plus losartan in infarcted ventricles. Isoproterenol also induced cardiac fibrosis, which was completely inhibited in infarcted rats by potassium canrenoate alone in right and left ventricles. In left ventricle, extent of fibrosis was, for control MI, 1.30 ± 0.34%; MI + iso, 2.50 ± 0.27%; MI + iso + pc, 0.82 ± 0.11%; and MI + iso + pc + los, 1.47 ± 0.31%. The deleterious effects of β-adrenoceptor stimulation on cardiac fibrosis seem therefore to involve aldosterone action. These results suggest a transregulation between the adrenergic and mineralocorticoid pathways, most likely at the nucleus level, with activation of profibrotic genes.
Persistent Identifierhttp://hdl.handle.net/10722/171311
ISSN
2015 Impact Factor: 2.462
2015 SCImago Journal Rankings: 0.962
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorBos, Ren_US
dc.contributor.authorMougenot, Nen_US
dc.contributor.authorFindji, Len_US
dc.contributor.authorMédiani, Oen_US
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorLechat, Pen_US
dc.date.accessioned2012-10-30T06:13:19Z-
dc.date.available2012-10-30T06:13:19Z-
dc.date.issued2005en_US
dc.identifier.citationJournal Of Cardiovascular Pharmacology, 2005, v. 45 n. 1, p. 8-13en_US
dc.identifier.issn0160-2446en_US
dc.identifier.urihttp://hdl.handle.net/10722/171311-
dc.description.abstractIn heart failure, the renin-angiotensin-aldosterone and the sympathetic systems are overactivated and lead to formation of cardiac fibrosis, which contributes to the aggravation of cardiac function. The aim of the present study was to evaluate the role of aldosterone and angiotensin II on formation of left ventricular fibrosis induced by chronic β-adrenergic stimulation with isoproterenol (iso) in the rat heart failure model induced by myocardial infarction (MI). Rats were submitted to chronic treatment with either the aldosterone receptor antagonist potassium canrenoate (pc, 20 mg/kg/d) or both aldosterone and angiotensin II receptor antagonists with addition of losartan (los, 10 mg/kg/d). Isoproterenol induced cardiac hypertrophy, which was completely inhibited by potassium canrenoate alone in atria and by potassium canrenoate plus losartan in infarcted ventricles. Isoproterenol also induced cardiac fibrosis, which was completely inhibited in infarcted rats by potassium canrenoate alone in right and left ventricles. In left ventricle, extent of fibrosis was, for control MI, 1.30 ± 0.34%; MI + iso, 2.50 ± 0.27%; MI + iso + pc, 0.82 ± 0.11%; and MI + iso + pc + los, 1.47 ± 0.31%. The deleterious effects of β-adrenoceptor stimulation on cardiac fibrosis seem therefore to involve aldosterone action. These results suggest a transregulation between the adrenergic and mineralocorticoid pathways, most likely at the nucleus level, with activation of profibrotic genes.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/en_US
dc.relation.ispartofJournal of Cardiovascular Pharmacologyen_US
dc.subject.meshAdrenergic Beta-Agonistsen_US
dc.subject.meshAldosterone - Physiologyen_US
dc.subject.meshAldosterone Antagonists - Pharmacologyen_US
dc.subject.meshAngiotensin Ii - Antagonists & Inhibitorsen_US
dc.subject.meshAngiotensin Ii Type 1 Receptor Blockers - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCanrenoate Potassium - Pharmacologyen_US
dc.subject.meshFibrosis - Chemically Induced - Prevention & Controlen_US
dc.subject.meshHeart Failure - Etiology - Pathology - Prevention & Controlen_US
dc.subject.meshIsoproterenolen_US
dc.subject.meshLosartan - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMyocardial Infarction - Complicationsen_US
dc.subject.meshMyocardium - Pathologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Wistaren_US
dc.subject.meshReceptors, Adrenergic, Beta - Physiologyen_US
dc.titleInhibition of catecholamine-induced cardiac fibrosis by an aldosterone antagonisten_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1097/00005344-200501000-00003en_US
dc.identifier.pmid15613973-
dc.identifier.scopuseid_2-s2.0-11144347913en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-11144347913&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume45en_US
dc.identifier.issue1en_US
dc.identifier.spage8en_US
dc.identifier.epage13en_US
dc.identifier.isiWOS:000225954000003-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridBos, R=7102085925en_US
dc.identifier.scopusauthoridMougenot, N=6602996596en_US
dc.identifier.scopusauthoridFindji, L=6507040549en_US
dc.identifier.scopusauthoridMédiani, O=6507974261en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridLechat, P=7102784631en_US

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