Document Detail


Aldosterone affects blood flow and vascular tone regulated by endothelium-derived NO: therapeutic implications.
MedLine Citation:
PMID:  23190073     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Aldosterone, in doses inappropriate to the salt status, plays an important role in the development of cardiovascular injury, including endothelial dysfunction, independent of its hypertensive effects. Acute non-genomic effects of aldosterone acting on mineralocorticoid receptors are inconsistent in healthy humans: vasoconstriction or forearm blood flow decrease via endothelial dysfunction, vasodilatation mediated by increased NO actions, or no effects. However, in studies with experimental animals, aldosterone mostly enhances vasodilatation mediated by endothelium-derived NO. Chronic exposure to aldosterone, which induces genomic responses, results in impairments of endothelial function through decreased NO synthesis and action in healthy individuals, experimental animals and isolated endothelial cells. Chronic aldosterone reduces NO release from isolated human endothelial cells only when extracellular sodium is raised. Oxidative stress is involved in the impairment of endothelial function by promoting NO degradation. Aldosterone liberates endothelin-1 (ET-1) from endothelial cells, which elicits ET(A) receptor-mediated vasoconstriction by inhibiting endothelial NO synthesis and action and through its own direct vasoconstrictor action. Ca(2+) flux through T-type Ca(2+) channels activates aldosterone synthesis and thus enhances unwanted effects of aldosterone on the endothelium. Mineralocorticoid receptor inhibitors, ET(A) receptor antagonists and T-type Ca(2) + channel blockers appear to diminish the pathophysiological participation of aldosterone in cardiovascular disease and exert beneficial actions on bioavailability of endothelium-derived NO, particularly in resistant hypertension and aldosteronism.
Authors:
Noboru Toda; Sadanobu Nakanishi; Shinichi Tanabe
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  British journal of pharmacology     Volume:  168     ISSN:  1476-5381     ISO Abbreviation:  Br. J. Pharmacol.     Publication Date:  2013 Feb 
Date Detail:
Created Date:  2013-01-17     Completed Date:  2013-07-02     Revised Date:  2014-02-04    
Medline Journal Info:
Nlm Unique ID:  7502536     Medline TA:  Br J Pharmacol     Country:  England    
Other Details:
Languages:  eng     Pagination:  519-33     Citation Subset:  IM    
Copyright Information:
© 2012 The Authors. British Journal of Pharmacology © 2012 The British Pharmacological Society.
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MeSH Terms
Descriptor/Qualifier:
Aldosterone / pharmacology,  physiology*
Animals
Blood Circulation
Endothelin-1 / metabolism
Endothelium, Vascular / physiology*
Humans
Nitric Oxide / metabolism
Nitric Oxide Synthase Type III / metabolism
Chemical
Reg. No./Substance:
0/Endothelin-1; 31C4KY9ESH/Nitric Oxide; 4964P6T9RB/Aldosterone; EC 1.14.13.39/Nitric Oxide Synthase Type III
Comments/Corrections

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