Document Detail


Chronic HgCl(2) treatment increases vasoconstriction induced by electrical field stimulation: role of adrenergic and nitrergic innervation.
MedLine Citation:
PMID:  21554244     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In the present study, we have investigated the possible changes in rat mesenteric artery vascular innervation function caused by chronic exposure to low doses of HgCl(2) (mercuric chloride), as well as the mechanisms involved. Rats were divided into two groups: (i) control, and (ii) HgCl(2)-treated rats (30 days; first dose, 4.6 μg/kg of body weight; subsequent dose, 0.07 μg·kg-1 of body weight·day-1, intramuscularly). Vasomotor response to EFS (electrical field stimulation), NA (noradrenaline) and the NO donor DEA-NO (diethylamine NONOate) were studied, nNOS (neuronal NO synthase) and phospho-nNOS protein expression were analysed, and NO, O(2)- (superoxide anion) and NA release were also determined. EFS-induced contraction was higher in the HgCl(2)-treated group. Phentolamine (1 μmol/l) decreased the response to EFS to a greater extent in HgCl(2)-treated rats. HgCl(2) treatment increased vasoconstrictor response to exogenous NA and NA release. L-NAME (N(G)-nitro-L-arginine methyl ester; 0.1 mmol/l) increased the response to EFS in both experimental groups, but the increase was greater in segments from control animals. HgCl(2) treatment decreased NO release and increased O(2)- production. Vasodilator response to DEA-NO was lower in HgCl(2)-treated animals. Tempol increased DEA-NO-induced relaxation to a greater extent in HgCl(2)-treated animals. nNOS expression was similar in arteries from both experimental groups, whereas phospho-nNOS was decreased in segments from HgCl(2)-treated animals. HgCl(2) treatment increased vasoconstrictor response to EFS as a result of, in part, reduced NO bioavailability and increased adrenergic function. These findings offer further evidence that mercury, even at low concentrations, is an environmental risk factor for cardiovascular disease.
Authors:
Javier Blanco-Rivero; Lorena B Furieri; Dalton V Vassallo; Mercedes Salaices; Gloria Balfagón
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Clinical science (London, England : 1979)     Volume:  121     ISSN:  1470-8736     ISO Abbreviation:  Clin. Sci.     Publication Date:  2011 Oct 
Date Detail:
Created Date:  2011-06-24     Completed Date:  2011-11-08     Revised Date:  2012-01-05    
Medline Journal Info:
Nlm Unique ID:  7905731     Medline TA:  Clin Sci (Lond)     Country:  England    
Other Details:
Languages:  eng     Pagination:  331-41     Citation Subset:  IM    
Affiliation:
Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma de Madrid, Madrid, Spain.
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MeSH Terms
Descriptor/Qualifier:
Acetylcholine / metabolism
Animals
Body Weight
Dose-Response Relationship, Drug
Electromagnetic Fields
Male
Mercuric Chloride / pharmacology*
Mesenteric Arteries / metabolism
Nitrergic Neurons / metabolism
Nitric Oxide / chemistry
Nitrogen / chemistry
Oxygen / chemistry
Rats
Rats, Wistar
Receptors, Adrenergic / metabolism
Vasoconstriction / drug effects*
Chemical
Reg. No./Substance:
0/Receptors, Adrenergic; 10102-43-9/Nitric Oxide; 51-84-3/Acetylcholine; 7487-94-7/Mercuric Chloride; 7727-37-9/Nitrogen; 7782-44-7/Oxygen

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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