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(Referência obtida automaticamente do Web of Science, por meio da informação sobre o financiamento pela FAPESP e o número do processo correspondente, incluída na publicação pelos autores.)

Reactive oxygen species derived from NAD(P) H oxidase play a role on ethanol-induced hypertension and endothelial dysfunction in rat resistance arteries

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Autor(es):
Simplicio, Janaina A. ; do Vale, Gabriel T. ; Gonzaga, Natalia A. ; Leite, Leticia N. ; Hipolito, Ulisses V. ; Pereira, Camila A. ; Tostes, Rita C. ; Tirapelli, Carlos R.
Número total de Autores: 8
Tipo de documento: Artigo Científico
Fonte: JOURNAL OF PHYSIOLOGY AND BIOCHEMISTRY; v. 73, n. 1, p. 5-16, FEB 2017.
Citações Web of Science: 11
Resumo

Chronic ethanol consumption is a risk factor for cardiovascular diseases. We studied whether NAD(P) H oxidasederived reactive oxygen species (ROS) play a role in ethanol-induced hypertension, vascular dysfunction, and protein expression in resistance arteries. Male Wistar rats were treated with ethanol (20 % v/v) for 6 weeks. Ethanol treatment increased blood pressure and decreased acetylcholine-induced relaxation in the rat mesenteric arterial bed (MAB). These responses were attenuated by apocynin (30 mg/kg/day; p. o. gavage). Ethanol consumption increased superoxide anion (O-2(-)) generation and decreased nitrate/nitrite (NOx) concentration in the rat MAB and apocynin prevented these responses. Conversely, ethanol did not affect the concentration of hydrogen peroxide (H2O2) and reduced glutathione (GSH) or the activity of superoxide dismutase (SOD) and catalase (CAT) in the rat MAB. Ethanol increased interleukin (IL)-10 levels in the rat MAB but did not affect the levels of tumor necrosis factor (TNF)-alpha, IL-6, or IL1 beta. Ethanol increased the expression of Nox2 and the phosphorylation of SAPK/JNK, but reduced eNOS expression in the rat MAB. Apocynin prevented these responses. However, ethanol treatment did not affect the expression of Nox1, Nox4, p38MAPK, ERK1/2, or SAPK/JNK in the rat MAB. Ethanol increased plasma levels of TBARS, TNF-alpha, IL-6, IL-1 beta, and IL-10, whereas it decreased NOx levels. The major finding of our study is that NAD(P) H oxidase-derived ROS play a role on ethanol-induced hypertension and endothelial dysfunction in resistance arteries. Moreover, ethanol consumption affects the expression and phosphorylation of proteins that regulate vascular function and NAD(P)H oxidase-derived ROS play a role in such responses. (AU)

Processo FAPESP: 13/03965-7 - Participação da NAD(P)H oxidase na disfunção vascular induzida pelo consumo crônico de etanol: relação com a sinalização redox e inflamação vascular.
Beneficiário:Ulisses Vilela Hipólito
Modalidade de apoio: Bolsas no Brasil - Pós-Doutorado
Processo FAPESP: 13/15824-9 - Participação da NAD(P)H oxidase na disfunção vascular e aumento da pressão arterial induzido pelo consumo de etanol: envolvimento do estresse oxidativo e da sinalização redox vascular
Beneficiário:Carlos Renato Tirapelli
Modalidade de apoio: Auxílio à Pesquisa - Regular