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- Publisher Website: 10.1097/00005344-200501000-00003
- Scopus: eid_2-s2.0-11144347913
- PMID: 15613973
- WOS: WOS:000225954000003
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Article: Inhibition of catecholamine-induced cardiac fibrosis by an aldosterone antagonist
Title | Inhibition of catecholamine-induced cardiac fibrosis by an aldosterone antagonist |
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Authors | |
Keywords | Aldosterone antagonist Angiotensin II antagonist Cardiac fibrosis Myocardial infarction β-adrenergic stimulation |
Issue Date | 2005 |
Publisher | Lippincott 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? |
Abstract | In 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 Identifier | http://hdl.handle.net/10722/171311 |
ISSN | 2023 Impact Factor: 2.6 2023 SCImago Journal Rankings: 0.610 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Bos, R | en_US |
dc.contributor.author | Mougenot, N | en_US |
dc.contributor.author | Findji, L | en_US |
dc.contributor.author | Médiani, O | en_US |
dc.contributor.author | Vanhoutte, PM | en_US |
dc.contributor.author | Lechat, P | en_US |
dc.date.accessioned | 2012-10-30T06:13:19Z | - |
dc.date.available | 2012-10-30T06:13:19Z | - |
dc.date.issued | 2005 | en_US |
dc.identifier.citation | Journal Of Cardiovascular Pharmacology, 2005, v. 45 n. 1, p. 8-13 | en_US |
dc.identifier.issn | 0160-2446 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/171311 | - |
dc.description.abstract | In 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.language | eng | en_US |
dc.publisher | Lippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/ | en_US |
dc.relation.ispartof | Journal of Cardiovascular Pharmacology | en_US |
dc.subject | Aldosterone antagonist | - |
dc.subject | Angiotensin II antagonist | - |
dc.subject | Cardiac fibrosis | - |
dc.subject | Myocardial infarction | - |
dc.subject | β-adrenergic stimulation | - |
dc.subject.mesh | Adrenergic Beta-Agonists | en_US |
dc.subject.mesh | Aldosterone - Physiology | en_US |
dc.subject.mesh | Aldosterone Antagonists - Pharmacology | en_US |
dc.subject.mesh | Angiotensin Ii - Antagonists & Inhibitors | en_US |
dc.subject.mesh | Angiotensin Ii Type 1 Receptor Blockers - Pharmacology | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Canrenoate Potassium - Pharmacology | en_US |
dc.subject.mesh | Fibrosis - Chemically Induced - Prevention & Control | en_US |
dc.subject.mesh | Heart Failure - Etiology - Pathology - Prevention & Control | en_US |
dc.subject.mesh | Isoproterenol | en_US |
dc.subject.mesh | Losartan - Pharmacology | en_US |
dc.subject.mesh | Male | en_US |
dc.subject.mesh | Myocardial Infarction - Complications | en_US |
dc.subject.mesh | Myocardium - Pathology | en_US |
dc.subject.mesh | Rats | en_US |
dc.subject.mesh | Rats, Wistar | en_US |
dc.subject.mesh | Receptors, Adrenergic, Beta - Physiology | en_US |
dc.title | Inhibition of catecholamine-induced cardiac fibrosis by an aldosterone antagonist | en_US |
dc.type | Article | en_US |
dc.identifier.email | Vanhoutte, PM:vanhoutt@hku.hk | en_US |
dc.identifier.authority | Vanhoutte, PM=rp00238 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1097/00005344-200501000-00003 | en_US |
dc.identifier.pmid | 15613973 | - |
dc.identifier.scopus | eid_2-s2.0-11144347913 | en_US |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-11144347913&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 45 | en_US |
dc.identifier.issue | 1 | en_US |
dc.identifier.spage | 8 | en_US |
dc.identifier.epage | 13 | en_US |
dc.identifier.isi | WOS:000225954000003 | - |
dc.publisher.place | United States | en_US |
dc.identifier.scopusauthorid | Bos, R=7102085925 | en_US |
dc.identifier.scopusauthorid | Mougenot, N=6602996596 | en_US |
dc.identifier.scopusauthorid | Findji, L=6507040549 | en_US |
dc.identifier.scopusauthorid | Médiani, O=6507974261 | en_US |
dc.identifier.scopusauthorid | Vanhoutte, PM=7202304247 | en_US |
dc.identifier.scopusauthorid | Lechat, P=7102784631 | en_US |
dc.identifier.issnl | 0160-2446 | - |