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Chronic lead exposure decreases the vascular reactivity of rat aortas: the role of hydrogen peroxide.

Nunes KZ, Nunes DO, Silveira EA, Almenara Cruz Pereira C, Broseghini Filho GB, Vassallo DV, Fioresi M - PLoS ONE (2015)

Bottom Line: Following N-nitro-L arginine methyl ester (L-NAME) 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 (SOD) administration.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiological Sciences, Federal University of Espírito Santo, Vitória, ES, Brazil.

ABSTRACT
We investigated whether exposure to small concentrations of lead alters blood pressure and vascular reactivity. Male 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 (1 nM-100 mM). Following N-nitro-L arginine methyl ester (L-NAME) 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 (SOD) administration. Catalase, diethyldithiocarbamic acid (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. Tetraethylammonium (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.

No MeSH data available.


Related in: MedlinePlus

Effects of the apocynin in endothelium-intact aortic segments from both untreated and lead-treated rats.Effects of the specific NAD(P)H oxidase inhibitor, apocynin (0.3 mM), on the concentration-response curves of phenylephrine in endothelium-intact aortic segments from both untreated and lead-treated rats. Each point represents the mean ± SEM. *p < 0.05 versus the corresponding control by Student’s t-test. The number of animals used is indicated in parentheses.
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pone.0120965.g007: Effects of the apocynin in endothelium-intact aortic segments from both untreated and lead-treated rats.Effects of the specific NAD(P)H oxidase inhibitor, apocynin (0.3 mM), on the concentration-response curves of phenylephrine in endothelium-intact aortic segments from both untreated and lead-treated rats. Each point represents the mean ± SEM. *p < 0.05 versus the corresponding control by Student’s t-test. The number of animals used is indicated in parentheses.

Mentions: In order to investigate whether NADPH oxidase was associated with increased levels of superoxide anions in lead-treated animals, we used apocynin (0.3 mM), an NADPH oxidase inhibitor. Apocynin reduced phenylephrine’s responsiveness in the untreated group, whereas the opposite response was observed in lead-treated animals, suggesting that this pathway may be involved in the production of superoxide anions and the subsequent production of hydrogen peroxide (Fig. 7).


Chronic lead exposure decreases the vascular reactivity of rat aortas: the role of hydrogen peroxide.

Nunes KZ, Nunes DO, Silveira EA, Almenara Cruz Pereira C, Broseghini Filho GB, Vassallo DV, Fioresi M - PLoS ONE (2015)

Effects of the apocynin in endothelium-intact aortic segments from both untreated and lead-treated rats.Effects of the specific NAD(P)H oxidase inhibitor, apocynin (0.3 mM), on the concentration-response curves of phenylephrine in endothelium-intact aortic segments from both untreated and lead-treated rats. Each point represents the mean ± SEM. *p < 0.05 versus the corresponding control by Student’s t-test. The number of animals used is indicated in parentheses.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4373949&req=5

pone.0120965.g007: Effects of the apocynin in endothelium-intact aortic segments from both untreated and lead-treated rats.Effects of the specific NAD(P)H oxidase inhibitor, apocynin (0.3 mM), on the concentration-response curves of phenylephrine in endothelium-intact aortic segments from both untreated and lead-treated rats. Each point represents the mean ± SEM. *p < 0.05 versus the corresponding control by Student’s t-test. The number of animals used is indicated in parentheses.
Mentions: In order to investigate whether NADPH oxidase was associated with increased levels of superoxide anions in lead-treated animals, we used apocynin (0.3 mM), an NADPH oxidase inhibitor. Apocynin reduced phenylephrine’s responsiveness in the untreated group, whereas the opposite response was observed in lead-treated animals, suggesting that this pathway may be involved in the production of superoxide anions and the subsequent production of hydrogen peroxide (Fig. 7).

Bottom Line: Following N-nitro-L arginine methyl ester (L-NAME) 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 (SOD) administration.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiological Sciences, Federal University of Espírito Santo, Vitória, ES, Brazil.

ABSTRACT
We investigated whether exposure to small concentrations of lead alters blood pressure and vascular reactivity. Male 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 (1 nM-100 mM). Following N-nitro-L arginine methyl ester (L-NAME) 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 (SOD) administration. Catalase, diethyldithiocarbamic acid (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. Tetraethylammonium (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.

No MeSH data available.


Related in: MedlinePlus