Chronic Lead Exposure Decreases the Vascular Reactivity of Rat Aortas: The Role of Hydrogen Peroxide
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 pr...
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Published in | PloS one Vol. 10; no. 3; p. e0120965 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
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United States
Public Library of Science
25.03.2015
Public Library of Science (PLoS) |
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Online Access | Get full text |
ISSN | 1932-6203 1932-6203 |
DOI | 10.1371/journal.pone.0120965 |
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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. |
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AbstractList | 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. 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.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. 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 R max 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. 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 [mu]g/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 R.sub.max 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. |
Audience | Academic |
Author | Fioresi, Mirian Nunes, Karolini Zuqui Cruz Pereira, Camila Almenara Vassallo, Dalton Valentim Nunes, Dieli Oliveira Silveira, Edna Aparecida Broseghini Filho, Gilson Brás |
AuthorAffiliation | University of Arkansas for Medical Sciences; College of Pharmacy, UNITED STATES 3 Health Science Centre of Vitória—EMESCAM, Vitória, Espírito Santo, Brazil 2 Department of Nursing, Federal University of Espírito Santo, Vitória, ES, Brazil 1 Department of Physiological Sciences, Federal University of Espírito Santo, Vitória, ES, Brazil |
AuthorAffiliation_xml | – name: 1 Department of Physiological Sciences, Federal University of Espírito Santo, Vitória, ES, Brazil – name: 3 Health Science Centre of Vitória—EMESCAM, Vitória, Espírito Santo, Brazil – name: 2 Department of Nursing, Federal University of Espírito Santo, Vitória, ES, Brazil – name: University of Arkansas for Medical Sciences; College of Pharmacy, UNITED STATES |
Author_xml | – sequence: 1 givenname: Karolini Zuqui surname: Nunes fullname: Nunes, Karolini Zuqui – sequence: 2 givenname: Dieli Oliveira surname: Nunes fullname: Nunes, Dieli Oliveira – sequence: 3 givenname: Edna Aparecida surname: Silveira fullname: Silveira, Edna Aparecida – sequence: 4 givenname: Camila Almenara surname: Cruz Pereira fullname: Cruz Pereira, Camila Almenara – sequence: 5 givenname: Gilson Brás surname: Broseghini Filho fullname: Broseghini Filho, Gilson Brás – sequence: 6 givenname: Dalton Valentim surname: Vassallo fullname: Vassallo, Dalton Valentim – sequence: 7 givenname: Mirian surname: Fioresi fullname: Fioresi, Mirian |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25807237$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_1016_j_tox_2020_152557 crossref_primary_10_1016_j_ejphar_2022_174950 crossref_primary_10_1016_j_taap_2016_10_023 crossref_primary_10_1007_s12012_016_9374_y crossref_primary_10_1016_j_clinsp_2023_100195 crossref_primary_10_1016_j_lfs_2017_05_009 crossref_primary_10_1007_s12011_018_1336_8 crossref_primary_10_1080_15287394_2018_1437490 crossref_primary_10_1016_j_envpol_2021_117942 crossref_primary_10_1007_s12011_016_0912_z |
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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Conceived and designed the experiments: KZN MF DVV. Performed the experiments: KZN DON CACP GBBF EAS. Analyzed the data: KZN MF DVV DON CACP GBBF EAS. Contributed reagents/materials/analysis tools: DVV EAS. Wrote the paper: KZN MF DVV EAS DON CACP GBBF. Competing Interests: The authors have declared that no competing interests exist. |
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SubjectTerms | Acetophenones - metabolism Animals Aorta Aorta - drug effects Aorta - metabolism Aorta - physiopathology Arginine Blood Blood levels Blood pressure Blood Pressure - drug effects Catalase Catalase - metabolism Chronic illnesses Contractility Ditiocarb - metabolism Drinking water Endothelium Exposure Hydrogen Hydrogen ion concentration Hydrogen peroxide Hydrogen Peroxide - metabolism Hypertension Incubation Kinases Laboratory animals Lead Lead - blood Lead - toxicity Lead content Legislation Male NG-Nitroarginine methyl ester NG-Nitroarginine Methyl Ester - pharmacology Nitric oxide Oxidative stress Oxidative Stress - drug effects Phenylephrine Phenylephrine - pharmacology Physiology Potassium Potassium channels Potassium Channels - metabolism Rats Rats, Wistar Reactive Oxygen Species - metabolism Reactivity Rodents Superoxide dismutase Superoxide Dismutase - pharmacology Superoxides Tetraethylammonium Tetraethylammonium - pharmacology Vasoconstriction - drug effects Vasoconstrictor Agents - pharmacology Vasodilation Vasodilator agents |
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Title | Chronic Lead Exposure Decreases the Vascular Reactivity of Rat Aortas: The Role of Hydrogen Peroxide |
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