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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.)

Ethanol withdrawal increases oxidative stress and reduces nitric oxide bioavailability in the vasculature of rats

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Author(s):
Gonzaga, Natalia A. [1, 2] ; Mecawi, Andre S. [3] ; Antunes-Rodrigues, Jose [3] ; De Martinis, Bruno S. [4] ; Padovan, Claudia M. [4] ; Tirapelli, Carlos R. [1]
Total Authors: 6
Affiliation:
[1] Univ Sao Paulo, Dept Enfermagem Psiquicitr & Ciencias Humanas, Escola Enfermagem Ribeirao Preto, Ribeirao Preto, SP - Brazil
[2] Univ Sao Paulo, Fac Med Ribeirao Preto, Programa Posgrad Farmacol, Ribeirao Preto, SP - Brazil
[3] Univ Sao Paulo, Dept Fisiol, Fac Med Ribeirao Preto, Ribeirao Preto, SP - Brazil
[4] Univ Sao Paulo, Fac Filosofia Ciencias & Letras Ribeirao Preto, Ribeirao Preto, SP - Brazil
Total Affiliations: 4
Document type: Journal article
Source: ALCOHOL; v. 49, n. 1, p. 47-56, FEB 2015.
Web of Science Citations: 22
Abstract

We analyzed the effects of ethanol withdrawal on the vascular and systemic renin-angiotensin system (RAS) and vascular oxidative stress. Male Wistar rats were treated with ethanol 3-9% (v/v) for a period of 21 days. Ethanol withdrawal was induced by abrupt discontinuation of the treatment. Experiments were performed 48 h after ethanol discontinuation. Rats from the ethanol withdrawal group showed decreased exploration of the open arms of the elevated-plus maze (EPM) and increased plasma corticosterone levels. Ethanol withdrawal significantly increased systolic blood pressure and plasma angiotensin II (ANG II) levels without an effect on plasma renin activity (PRA), angiotensin converting enzyme (ACE) activity, or plasma angiotensin I (ANG I) levels. No differences in vascular ANG I, ANG II levels, and ACE activity/expression and AT(1) and AT(2) receptor expression were detected among the experimental groups. Plasma osmolality, as well as plasma sodium, potassium, and glucose levels were not affected by ethanol withdrawal. Ethanol withdrawal induced systemic and vascular oxidative stress, as evidenced by increased plasma thiobarbituric acid-reacting substances (TBARS) levels and the vascular generation of superoxide anion. Ethanol withdrawal significantly decreased plasma and vascular nitrate/nitrite levels. Major new findings of the present study are that ethanol withdrawal induces vascular oxidative stress and reduces nitric oxide (NO) levels in the vasculature. Additionally, our study provides novel evidence that ethanol withdrawal does not affect the vascular ANG II generating system while stimulating systemic RAS. These responses could predispose individuals to the development of cardiovascular diseases. (C) 2015 Elsevier Inc. All rights reserved. (AU)

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 Opportunities: Regular Research Grants
FAPESP's process: 13/00808-8 - Consequences of ethanol withdrawal on the vasculature and the systemic and local renin-angiotensin system (ras)
Grantee:Carlos Renato Tirapelli
Support Opportunities: Regular Research Grants