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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.)

Tumor necrosis factor-alpha receptor 1 contributes to ethanol-induced vascular reactive oxygen species generation and hypertension

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Autor(es):
Simplicio, Janaina A. [1, 2] ; Gonzaga, Natalia A. [1, 2] ; Nakashima, Marcelo A. [2] ; De Martinis, Bruno S. [3] ; Cunha, Thiago M. [1] ; Tirapelli, Luis F. [4] ; Tirapelli, Carlos R. [2]
Número total de Autores: 7
Afiliação do(s) autor(es):
[1] Univ Sao Paulo, Fac Med Ribeirao Preto, Programa Posgrad Farmacol, Ribeirao Preto, SP - Brazil
[2] Univ Sao Paulo, Escola Enfermagem Ribeirao Preto, Lab Farmacol, Ave Bandeirantes 3900, BR-14040902 Ribeirao Preto, SP - Brazil
[3] Univ Sao Paulo, Fac Filosofia Ciencias & Letras Ribeirao Preto, Ribeirao Preto, SP - Brazil
[4] Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Cirurgia & Anat, Ribeirao Preto, SP - Brazil
Número total de Afiliações: 4
Tipo de documento: Artigo Científico
Fonte: JOURNAL OF THE AMERICAN SOCIETY OF HYPERTENSION; v. 11, n. 10, p. 684-696, OCT 2017.
Citações Web of Science: 7
Resumo

We evaluated the contribution of tumor necrosis factor-alpha receptor 1 (TNFR1) to ethanol-induced hypertension and vascular oxidative stress and the possible role of perivascular adipose tissue (PVAT) in such responses. Male C57BL/6 wild-type (WT) or TNFR1-deficient mice (TNFR1(-/-)) were treated with ethanol (20% vol/vol) for 12 weeks. Ethanol induced an increase in blood pressure in WT mice and TNFR1(-/-) at 4 and 5 weeks of treatment, respectively. Treatment with ethanol increased tumor necrosis factor-alpha and interleukin-6 levels in aortas with or without PVAT (PVAT+ and PVAT-, respectively) from WT mice, but not TNFR1(-/-). Ethanol increased superoxide anion (O-2(-)) generation, thiobarbituric acid reactive substance concentration, and the activity of superoxide dismutase and catalase in aortas (PVAT- and PVAT+) from WT mice, but not TNFR1(-/-). Conversely, ethanol consumption decreased the concentration of nitrate/nitrite in aortas (PVAT- and PVAT+) from WT mice, but not TNFR1(-/-). Treatment with ethanol increased myeloperoxidase activity in aortas (PVAT- and PVAT+) from WT mice, but not TNFR1(-/-). The major finding of our study is that TNFR1 contributes to ethanol-induced hypertension and oxidative stress in the vasculature. Additionally, TNFR1 plays a role in ethanol-induced increase in proinflammatory cytokines and neutrophils migration. However, PVAT does not counteract or aggravate the effects induced by ethanol. (C) 2017 American Society of Hypertension. All rights reserved. (AU)

Processo FAPESP: 14/09595-0 - Participação do TNF-alfa nas disfunções vasculares induzidas pelo consumo crônico de etanol: envolvimento do tecido adiposo perivascular
Beneficiário:Janaina Aparecida Simplicio
Linha de fomento: Bolsas no Brasil - Doutorado