| Molecular mechanisms of myocardial remodeling. The role of aldosterone. | |
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MedLine Citation:
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PMID: 12505056 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Cardiac remodeling, CR, is a complex and rather controversial issue and results from the, sometimes opposite, trophic effects of pure mechanical overload, and susceptibility factors, as senescence, aetiologies, as ischemia, and the neurohormonal reaction. The molecular mechanisms of CR are heritable and had, in the past, increased fitness, as such CR belongs to evolutionary medicine. Aldosterone production plays an important role in the remodeling of the heart. (i) There are numerous evidences that aldosterone induces fibrosis in all the cardiovascular system in the presence of high sodium diet. The aldosterone receptor is a transcriptional factor and the pathways that lead to aldosterone-induced fibrosis are multiple. Aldosterone induces the expression of the angiotensin II receptors subtype I and that of the glucocorticoid receptors. The RALES trial have recently evidenced a significant beneficial effect of spironolactone on both mortality and morbidity in heart failure, and a substudy has shown that these effects are linked to a reduction is fibrosis. (ii) An intracardiac production of aldosterone and corticosterone have been evidenced in the rat. Aldosterone production is regulated by low sodium/high potassium diets and by angiotensin II and is predominant in atria, cardiac production is low as compared to the adrenal production, nevertheless it results in high local concentrations, just like angiotensin II. In rats, myocardial infarction activates aldosterone production and this activation is prevented by losartan. Heart failure, in human, activates aldosterone production and is accompanied by a significant increase of the arteriovenous difference in aldosterone by the myocardium. To conclude (i) after a myocardial infarction local production of aldosterone and angiotensin II are likely to play a major role in regulating collagen turnover and fibrous tissue formation; (ii) during heart failure, the activation of adrenal and cardiovascular production of aldosterone belongs to the neurohormonal reaction and would play a detrimental role in producing reactive fibrosis. |
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Authors:
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Claude Delcayre; Bernard Swynghedauw |
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Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: Journal of molecular and cellular cardiology Volume: 34 ISSN: 0022-2828 ISO Abbreviation: J. Mol. Cell. Cardiol. Publication Date: 2002 Dec |
Date Detail:
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Created Date: 2002-12-30 Completed Date: 2003-07-14 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0262322 Medline TA: J Mol Cell Cardiol Country: England |
Other Details:
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Languages: eng Pagination: 1577-84 Citation Subset: IM |
Affiliation:
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CD Directeur de Recherches au CNRS, U217-INSERM, Hôpital Lariboisière, Paris, France. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Aldosterone
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physiology*,
secretion Animals Cardiomyopathies / metabolism, pathology* Female Fibrosis Heart Failure / metabolism, pathology Humans Mice Mice, Transgenic Myocardial Ischemia / metabolism, pathology Myocardium / metabolism, pathology Rats Ventricular Remodeling |
| Chemical | |
Reg. No./Substance:
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52-39-1/Aldosterone |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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