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This Article Full Text Full Text (PDF) All Versions of this Article: 295/3/H1033    most recent 00430.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Wiggers, G. A. Articles by Salaices, M. Search for Related Content PubMed PubMed Citation Articles by Wiggers, G. A. Articles by Salaices, M.

Low mercury concentrations cause oxidative stress and endothelial dysfunction in conductance and resistance arteries

¹Departamento de Farmacología, Universidad Autónoma de Madrid; ²Departamento de Ciencias de la Salud III, Universidad Rey Juan Carlos, Alcorcón; ³Departamento de Fisiología, Universidad Complutense de Madrid, Madrid, Spain; and ⁴Departamento de Ciências Fisiológicas, Universidade Federal do Espírito Santo, Vitória, Brazil

Submitted 24 April 2008 ; accepted in final form 27 June 2008

Increased cardiovascular risk after mercury exposure has been described, but the underlying mechanisms are not well explored. We analyzed the effects of chronic exposure to low mercury concentrations on endothelium-dependent responses in aorta and mesenteric resistance arteries (MRA). Wistar rats were treated with mercury chloride (1st dose 4.6 µg/kg, subsequent dose 0.07 µg·kg^–1·day^–1 im, 30 days) or vehicle. Blood levels at the end of treatment were 7.97 ± 0.59 ng/ml. Mercury treatment: 1) did not affect systolic blood pressure; 2) increased phenylephrine-induced vasoconstriction; 3) reduced acetylcholine-induced vasodilatation; and 4) reduced in aorta and abolished in MRA the increased phenylephrine responses induced by either endothelium removal or the nitric oxide synthase (NOS) inhibitor N^G-nitro-L-arginine methyl ester (L-NAME, 100 µM). Superoxide dismutase (SOD, 150 U/ml) and the NADPH oxidase inhibitor apocynin (0.3 mM) decreased the phenylephrine-induced contraction in aorta more in mercury-treated rats than controls. In MRA, SOD did not affect phenylephrine responses; however, when coincubated with L-NAME, the L-NAME effect on phenylephrine response was restored in mercury-treated rats. Both apocynin and SOD restored the impaired acetylcholine-induced vasodilatation in vessels from treated rats. Endothelial NOS expression did not change in aorta but was increased in MRA from mercury-treated rats. Vascular O₂^– production, plasmatic malondialdehyde levels, and total antioxidant status increased with the mercury treatment. In conclusion, chronic exposure to low concentrations of mercury promotes endothelial dysfunction as a result of the decreased NO bioavailability induced by increases in oxidative stress. These findings offer further evidence that mercury, even at low concentrations, is an environmental risk factor for cardiovascular disease.

mercury; oxidative stress; nitric oxide; arteries

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