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

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]

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

• 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
• Modalidade de apoio: Bolsas no Brasil - Doutorado