AJP - Heart Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Heart Circ Physiol 295: H1033-H1043, 2008. First published July 3, 2008; doi:10.1152/ajpheart.00430.2008
0363-6135/08 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
295/3/H1033    most recent
00430.2008v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Google Scholar
Right arrow Articles by Wiggers, G. A.
Right arrow Articles by Salaices, M.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wiggers, G. A.
Right arrow Articles by Salaices, M.

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

G. A. Wiggers,1,4,* F. M. Peçanha,1,4,* A. M. Briones,1 J. V. Pérez-Girón,2 M. Miguel,1 D. V. Vassallo,4 V. Cachofeiro,3 M. J. Alonso,1,2 and M. Salaices1

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 NG-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


Address for reprint requests and other correspondence: M. Salaices, Departamento de Farmacología, Universidad Autónoma de Madrid, Arzobispo Morcillo 4, 28029 Madrid, Spain (e-mail: mercedes.salaices{at}uam.es)






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2008 by the American Physiological Society.