Perinatal lead exposure affects nitric oxide and cyclooxygenase pathways in aorta of weaned rats

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dc.contributor.authorGrizzo, Larissa Tercilia [UNESP]
dc.contributor.authorCordellini, Sandra [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-20T13:49:14Z
dc.date.available2014-05-20T13:49:14Z
dc.date.issued2008-05-01
dc.description.abstractPerinatal Pb exposure may modulate arterial tone through nitric oxide (NO) and cyclooxygenase products. To investigate this, Wistar dams received 1000 ppm of Pb or sodium acetate (control) in drinking water during pregnancy and lactation. Curves were constructed in phenylephrine-precontracted intact and/or denuded rings of thoracic aortas of weaned (23-day-old) male pups from their responses to N-omega-nitro-L-arginine methyl ester (L-NAME, NO synthase inhibitor) and ACh in the absence or presence of indomethacin (10(-5)M, cyclooxygenase inhibitor) or L-NAME (3 x 10(-7)M and 3 x 10(-4)M). Blood lead concentration and systolic blood pressure (SBP) were higher in intoxicated than control pups (blood lead mu g/dl: control < 3.0, Pb 58.7 +/- 6.5*; SBP mmHg: control 111.4 +/- 2.3, Pb 135.5 +/- 2.4*). In L-NAME-treated rings maximal responses increased in Pb-exposed rats, and were higher in intact than in denuded aortas (contraction [% of phenylephrine] intact: control 184.3 +/- 23.7, Pb 289.1 +/- 18.3*; denuded: control 125.1 +/- 4.5, Pb 154.8 +/- 13.3*). ACh-induced relaxation in intact aortas from Pb-exposed rats presented rightward shift in L-NAME presence (EC50 x 10(-7)M: control 1.32 [0.33-5.18], Pb 4.88 [3.56-6.69]*) but moved left under indomethacin (EC50 x 10(-7)M: control 8.95 [3.47-23.07], Pb 0.97 [0.38-2.43]*). *p < 0.05 significant relative to the respective control; N = 7-9. Endothelium removal abolished ACh-induced relaxation. Perinatal Pb exposure caused hypertension associated with alterations in the production and/or release of basal and stimulated endothelium-derived relaxing factors-NO and constricting cyclooxygenase products. These findings may help explain the contribution of NO and cyclooxygenase products to the etiology and/or maintenance of Pb-induced hypertension and could ultimately lead to therapeutic advantages in plumbism.en
dc.description.affiliationUNESP, São Paulo State Univ, Inst Biociencias, Dept Farmacol, BR-18618000 Botucatu, SP, Brazil
dc.description.affiliationUnespUNESP, São Paulo State Univ, Inst Biociencias, Dept Farmacol, BR-18618000 Botucatu, SP, Brazil
dc.format.extent207-214
dc.identifierhttp://dx.doi.org/10.1093/toxsci/kfn018
dc.identifier.citationToxicological Sciences. Oxford: Oxford Univ Press, v. 103, n. 1, p. 207-214, 2008.
dc.identifier.doi10.1093/toxsci/kfn018
dc.identifier.issn1096-6080
dc.identifier.lattes5616488317690037
dc.identifier.urihttp://hdl.handle.net/11449/17531
dc.identifier.wosWOS:000254955500021
dc.language.isoeng
dc.publisherOxford University Press
dc.relation.ispartofToxicological Sciences
dc.relation.ispartofjcr4.181
dc.relation.ispartofsjr1,538
dc.rights.accessRightsAcesso restrito
dc.sourceWeb of Science
dc.subjectmetalsen
dc.subjectdevelopmental toxicologyen
dc.subjectcardiovascular systemen
dc.subjectendothelial factorsen
dc.subjectperinatal intoxicationen
dc.subjectweaned ratsen
dc.titlePerinatal lead exposure affects nitric oxide and cyclooxygenase pathways in aorta of weaned ratsen
dc.typeArtigo
dcterms.licensehttp://www.oxfordjournals.org/access_purchase/self-archiving_policyb.html
dcterms.rightsHolderOxford Univ Press
unesp.author.lattes5616488317690037
unesp.campusUniversidade Estadual Paulista (Unesp), Instituto de Biociências, Botucatupt

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