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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

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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Author(s):
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.
Total Authors: 8
Document type: Journal article
Source: JOURNAL OF PHYSIOLOGY AND BIOCHEMISTRY; v. 73, n. 1, p. 5-16, FEB 2017.
Web of Science Citations: 11
Abstract

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)

FAPESP's process: 13/03965-7 - Involvement of NAD(P)H oxidase in vascular dysfunction induced by chronic ethanol consumption: relationship to redox signaling and vascular inflamation
Grantee:Ulisses Vilela Hipólito
Support type: Scholarships in Brazil - Post-Doctorate
FAPESP's process: 13/15824-9 - Role of NAD(P)H oxidase in vascular dysfunction and increased blood pressure induced by ethanol consumption: involvement of oxidative stress and the vascular redox signaling
Grantee:Carlos Renato Tirapelli
Support type: Regular Research Grants