Perivascular adipose tissue protects against the vascular dysfunction induced by acute ethanol intake: Role of hydrogen peroxide

Author(s)

Gonzaga, Natalia A. ^{[1, 2]} ; Awata, Wanessa M. C. ^{[1, 2]} ; do Vale, Gabriel T. ^{[1, 2]} ; Marchi, Katia C. ^{[1, 2]} ; Muniz, Jaqueline J. ^[2] ; Tanus-Santos, Jose E. ^[1] ; Tirapelli, Carlos R. ^[2]

Affiliation

^[1] Univ Sao Paulo, Fac Med Ribeirao Preto, Programa Posgrad Farmacol, Ribeirao Preto, SP - Brazil

^[2] Univ Sao Paulo, Escola Enfermagem Ribeirao Preto, DEPCH, Lab Farmacol, Ribeirao Preto, SP - Brazil

• Document type: Journal article
• Source: VASCULAR PHARMACOLOGY; v. 111, p. 44-53, DEC 2018.
• Web of Science Citations: 1

Abstract

Aim: We investigated the consequences of acute ethanol intake on the anti-contractile effect of perivascular adipose tissue (PVAT). Methods: The effects of a single dose of ethanol (1 g/kg; p.o. gavage) on the vascular function were assessed within 30 min in male Wistar rats. Results: Ethanol decreased the relaxation induced by acetylcholine and increased the contraction induced by phenylephrine in endothelium-intact, but not in endothelium-denuded aortas without PVAT. The vascular dysfunction induced by ethanol was not observed in aortic rings with PVAT. N-omega-Nitro-l-arginine methyl ester (L-NAME), NG-nitro-L-arginine (L-NNA) and 1H-(1,2,4)oxadiazolo{[}4,3-a]quinoxalin-1-one (ODQ), but not tiron or tempo], increased the contraction induced by phenylephrine in endothelium-intact aortas with PVAT from control and ethanol-treated rats. Catalase increased phenylephrine-induced contraction in aortas with PVAT from ethanol-treated rats, but not from control rats. Conversely, inhibition of catalase with aminotriazole decreased phenylephrine-induced contraction in aortas from ethanol-treated rats. Treatment with ethanol increased hydrogen peroxide (H2O2) levels and decreased catalase activity in aortas with PVAT. Ethanol increased superoxide anion (O-2(-)) generation in aortas with or without PVAT. Superoxide dismutase (SOD) activity was not affected by ethanol intake. In situ quantification of H2O2 using 2'7'dichlorodihydrofluorescein diacetate (DCFH-DA) revealed increased levels of H2O2 in periaortic PVAT from ethanol-treated rats. However, in situ evaluation of nitric oxide (NO) in both aorta and PVAT showed no differences between groups. Conclusions: Our study provides novel evidence that the periaortic PVAT protects against the vascular dysfunction induced by acute ethanol intake through a mechanism that involves increased generation of H2O2. (AU)

• FAPESP's process: 10/05815-4 - Assessment of the role of angiotensin II in the cardiovascular effects induced by acute ethanol consumption
• Grantee: Carlos Renato Tirapelli
• Support Opportunities: Regular Research Grants