| Review of aldosterone- and angiotensin II-induced target organ damage and prevention. | |
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MedLine Citation:
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PMID: 14985063 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Aldosterone is well recognized as a cause of sodium reabsorption, water retention, and potassium and magnesium loss; however, it also produces a variety of other actions that lead to progressive target organ damage in the heart, vasculature, and kidneys. Aldosterone interacts with mineralocorticoid receptors to promote endothelial dysfunction, facilitate thrombosis, reduce vascular compliance, impair baroreceptor function, and cause myocardial and vascular fibrosis. Although angiotensin II has been considered the major mediator of cardiovascular damage, increasing evidence suggests that aldosterone may mediate and exacerbate the damaging effects of angiotensin II. While angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers reduce plasma aldosterone levels initially, aldosterone rebound, or 'escape' may occur during long-term therapy. Therefore, aldosterone blockade is required to reduce the risk of progressive target organ damage in patients with hypertension and heart failure. This may be achieved nonselectively with spironolactone or with use of the selective aldosterone blocker eplerenone. While both agents have been demonstrated to be effective antihypertensive agents, eplerenone may produce improved target organ protection as witnessed in a variety of clinical settings, without the antiandrogenic and progestational effects commonly observed with spironolactone. |
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Authors:
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Allan D Struthers; Thomas M MacDonald |
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Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: Cardiovascular research Volume: 61 ISSN: 0008-6363 ISO Abbreviation: Cardiovasc. Res. Publication Date: 2004 Mar |
Date Detail:
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Created Date: 2004-02-26 Completed Date: 2004-07-12 Revised Date: 2004-11-17 |
Medline Journal Info:
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Nlm Unique ID: 0077427 Medline TA: Cardiovasc Res Country: Netherlands |
Other Details:
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Languages: eng Pagination: 663-70 Citation Subset: IM |
Affiliation:
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Department of Clinical Pharmacology and Therapeutics, Ninewells Hospital and Medical School, Tayside DD1 9SY, Dundee, UK. a.d.struthers@dundee.ac.uk |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Aldosterone
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physiology* Aldosterone Antagonists / therapeutic use Angiotensin II / physiology* Angiotensin-Converting Enzyme Inhibitors / therapeutic use Animals Cardiovascular Diseases / drug therapy, metabolism* Endothelium, Vascular / metabolism Humans Kidney / metabolism Myocardium / metabolism* Receptor, Angiotensin, Type 2 / antagonists & inhibitors Spironolactone / analogs & derivatives*, therapeutic use |
| Chemical | |
Reg. No./Substance:
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0/Aldosterone Antagonists; 0/Angiotensin-Converting Enzyme Inhibitors; 0/Receptor, Angiotensin, Type 2; 0/eplerenone; 11128-99-7/Angiotensin II; 52-01-7/Spironolactone; 52-39-1/Aldosterone |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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