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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 blood pressure and vascular oxidative stress: a role for angiotensin type 1 receptors

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Author(s):
Gonzaga, Natalia A. [1, 2] ; do Vale, Gabriel T. [1, 2] ; Parente, Juliana M. [1] ; Yokota, Rodrigo [3] ; De Martinis, Bruno S. [4] ; Casarini, Dulce E. [3] ; Castro, Michele M. [1] ; Tirapelli, Carlos R. [2]
Total Authors: 8
Affiliation:
[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, DEPCH, Ribeirao Preto, SP - Brazil
[3] Univ Fed Sao Paulo, Escola Paulista Med, Dept Med, Div Nefrol, Sao Paulo - Brazil
[4] Univ Sao Paulo, Fac Filosofia Ciencias & Letras Ribeirao Preto, Ribeirao Preto, SP - Brazil
Total Affiliations: 4
Document type: Journal article
Source: JOURNAL OF THE AMERICAN SOCIETY OF HYPERTENSION; v. 12, n. 7, p. 561-573, JUL 2018.
Web of Science Citations: 2
Abstract

We evaluated the possible mechanisms underlying the oxidative stress induced by ethanol withdrawal. With this purpose, we verified the role of AT(1) receptors in such response. Male Wistar rats were treated with ethanol 3%-9% (vol./vol.) for 21 days. Ethanol withdrawal was induced by abrupt discontinuation of the treatment. Experiments were performed 48 hours after ethanol discontinuation. Increased plasma levels of angiotensin II were detected after ethanol withdrawal. Losartan (10 mg/kg; p.o. gavage), a selective AT(1) receptor antagonist, impeded the increase in blood pressure induced by ethanol withdrawal. Increased lipoperoxidation and superoxide anion (O-2(-)) levels were detected in aortas after ethanol withdrawal, and losartan prevented these responses. Decreased hydrogen peroxide and nitrate/nitrite concentration were detected in aortas after ethanol withdrawal, and losartan prevented these effects. Nitrotyrosine immunostaining in the rat aorta was increased after ethanol withdrawal, and AT(1) blockade impeded this response. Increased expression of PKC delta and p47(phox) was detected after ethanol withdrawal, and treatment with losartan prevented these responses. Our study provides novel evidence that ethanol withdrawal increases vascular oxidative stress and blood pressure through AT(1)-dependent mechanisms. These findings highlight the importance of angiotensin II in ethanol withdrawal-induced increase in blood pressure and vascular oxidative damage. (C) 2018 American Heart Association. All rights reserved. (AU)

FAPESP's process: 15/22046-8 - Role of AT1 receptors on ethanol withdrawal-induced hypertension and vascular oxidative stress
Grantee:Carlos Renato Tirapelli
Support Opportunities: Regular Research Grants