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dc.contributor.authorFiorim, Jonaína
dc.contributor.authorRibeiro, Rogério Faustino
dc.contributor.authorSilveira, Edna Aparecida Parecida
dc.contributor.authorPadilha, Alessandra Simão
dc.contributor.authorVescovi, Marcos Vinícius Altoé
dc.contributor.authorDe Jesus, Honério Coutinho
dc.contributor.authorStefanon, Ivanita
dc.contributor.authorSalaices Sánchez, Mercedes 
dc.contributor.authorVassallo, Dalton Valentim
dc.contributor.otherUAM. Departamento de Farmacologíaes_ES
dc.date.accessioned2015-04-30T07:30:53Z
dc.date.available2015-04-30T07:30:53Z
dc.date.issued2011-03-07
dc.identifier.citationPlos One 6.2 (2011): e17117en_US
dc.identifier.issn1932-6203 (online)en_US
dc.identifier.urihttp://hdl.handle.net/10486/665683
dc.description.abstractChronic lead exposure induces hypertension and alters endothelial function. However, treatment with low lead concentrations was not yet explored. We analyzed the effects of 7 day exposure to low lead concentrations on endothelium-dependent responses. Wistar rats were treated with lead (1st dose 4 μg/100 g, subsequent dose 0.05 μg/100 g, i.m. to cover daily loss) or vehicle; blood levels attained at the end of treatment were 9.98 μg/dL. Lead treatment had the following effects: increase in systolic blood pressure (SBP); reduction of contractile response to phenylephrine (1 nM-100 μM) of aortic rings; unaffected relaxation induced by acetylcholine (0.1 nM-300 μM) or sodium nitroprusside (0.01 nM-0.3 μM). Endothelium removal, NG-nitro-L-arginine methyl ester (100 μM) and tetraethylammonium (2 mM) increased the response to phenylephrine in treated rats more than in untreated rats. Aminoguanidine (50 μM) increased but losartan (10 μM) and enalapril (10 μM) reduced the response to phenylephrine in treated rats. Lead treatment also increased aortic Na+/K+-ATPase functional activity, plasma angiotensin-converting enzyme (ACE) activity, protein expression of the Na+/K+-ATPase alpha-1 subunit, phosphorylated endothelial nitric oxide synthase (p-eNOS), and inducible nitric oxide synthase (iNOS). Our results suggest that on initial stages of lead exposure, increased SBP is caused by the increase in plasma ACE activity. This effect is accompanied by increased p-eNOS, iNOS protein expression and Na+/K+-ATPase functional activity. These factors might be a compensatory mechanism to the increase in SBPen_US
dc.description.sponsorshipThis study was supported by grants from CAPES (Coordenação de Aperfeiçoamento Pessoal de Nível Superior) and CNPq (Conselho Nacional de desenvolvimento Científico e Tecnológico)/FAPES (Fundação de Apoio à Pesquisa do Espírito Santo)/FUNCITEC (Fundação de Ciência e Tecnologia) (39767531/07), Brazil and from MCINN (SAF 2009-07201) and ISCIII (Red RECAVA, RD06/0014/0011), Spainen_US
dc.format.extent9 pag.es_ES
dc.format.mimetypeapplication/pdfen
dc.language.isoengen
dc.publisherPublic Library of Scienceen_US
dc.relation.ispartofPlos Oneen_US
dc.rights© 2011 Fiorim et al.es_ES
dc.subject.otherAortaes_ES
dc.subject.otherBlood Pressureen_US
dc.subject.otherRatsen_US
dc.subject.otherEndothelium, Vascularen_US
dc.subject.otherLead Poisoninges_ES
dc.subject.otherVasoconstrictionen_US
dc.titleLow-level lead exposure increases systolic arterial pressure and endothelium-derived vasodilator factors in rat aortasen_US
dc.typearticleen
dc.subject.ecienciaMedicinaes_ES
dc.identifier.doi10.1371/journal.pone.0017117es_ES
dc.identifier.publicationfirstpagee17117es_ES
dc.identifier.publicationissue2es_ES
dc.identifier.publicationlastpagee17117es_ES
dc.identifier.publicationvolume6es_ES
dc.type.versioninfo:eu-repo/semantics/publishedVersionen
dc.rights.ccReconocimientoes_ES
dc.rights.accessRightsopenAccessen
dc.authorUAMSalaices Sánchez, Mercedes (260920)
dc.facultadUAMFacultad de Medicina


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