Ciências Fisiológicas

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Navegando Ciências Fisiológicas por Assunto "Acetato de chumbo"

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    A exposição crônica ao chumbo diminui a reatividade vascular em aorta de ratos: papel do peróxido de hidrogênio
    (Universidade Federal do Espírito Santo, 2014-12-17) Nunes, Karolini Zuqui; Fioresi, Mirian; Vassallo, Dalton Valentim; Gouvea, Sonia Alves; Moyses, Margareth Ribeiro; Peçanha, Giulia Alessandra Wiggers
    We investigated whether exposure to small concentrations of lead alters blood pressure and vascular reactivity.Wistar rats were sorted randomly into the following two groups: control (Ct) and treatment with 100 ppm of lead (Pb), which was added to drinking water, for 30 days. Systolic blood pressure (BP) was measured weekly. Following treatment, aortic ring vascular reactivity was assessed. Tissue samples were properly stored for further biochemical investigation. The lead concentration in the blood reached approximately 8 µg/dL. Treatment increased blood pressure and decreased the contractile responses of the aortic rings to phenylephrine. Following LNAME administration, contractile responses increased in both groups but did not differ significantly between them. Lead effects on Rmax were decreased compared to control subjects following superoxide dismutase administration, Catalase, DETCA, and apocynin increased the vasoconstrictor response induced by phenylephrine in the aortas of lead-treated rats but did not increase the vasoconstrictor response in the aortas of untreated rats. TEA potentiated the vasoconstrictor response induced by phenylephrine in aortic segments in both groups, but these effects were greater in lead-treated rats. The co-incubation of TEA and catalase abolished the vasodilatory effect noted in the lead group. The present study is the first to demonstrate that blood lead concentrations well below the values established by international legislation increased blood pressure and decreased phenylephrine-induced vascular reactivity. The latter effect was associated with oxidative stress, specifically oxidative stress induced via increases in hydrogen peroxide levels and the subsequent effects of hydrogen peroxide on potassium channels.