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Acute ethanol intake induces superoxide anion generation and mitogen-activated protein kinase phosphorylation in rat aorta: A role for angiotensin type 1 receptor

Yogi, Alvaro ; Callera, Glaucia E. ; Mecawi, André S. ; Batalhão, Marcelo E. ; Carnio, Evelin C. ; Antunes-Rodrigues, José ; Queiroz, Regina H. ; Touyz, Rhian M. ; Tirapelli, Carlos R.

Toxicology and applied pharmacology, 2012-11, Vol.264 (3), p.470-478 [Periódico revisado por pares]

Amsterdam: Elsevier Inc

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Título:
Acute ethanol intake induces superoxide anion generation and mitogen-activated protein kinase phosphorylation in rat aorta: A role for angiotensin type 1 receptor
Autor: Yogi, Alvaro ; Callera, Glaucia E. ; Mecawi, André S. ; Batalhão, Marcelo E. ; Carnio, Evelin C. ; Antunes-Rodrigues, José ; Queiroz, Regina H. ; Touyz, Rhian M. ; Tirapelli, Carlos R.
Assuntos: 60 APPLIED LIFE SCIENCES ; ACETYLCHOLINE ; Alcoholism and acute alcohol poisoning ; ANGIOTENSIN ; Angiotensin I ; Angiotensin II ; Angiotensin II Type 1 Receptor Blockers - administration & dosage ; Angiotensin II Type 1 Receptor Blockers - pharmacology ; Animals ; ANIONS ; AORTA ; Aorta - drug effects ; Aorta - metabolism ; Biological and medical sciences ; BLOOD PRESSURE ; Blood Pressure - drug effects ; c-Jun amino-terminal kinase ; Cytosol ; DAMAGE ; ENDOTHELIUM ; ETHANOL ; Ethanol - administration & dosage ; Ethanol - blood ; Ethanol - toxicity ; Gene Expression Regulation - drug effects ; INJURIES ; INTAKE ; Losartan ; Losartan - administration & dosage ; Losartan - pharmacology ; Male ; MAP kinase ; Medical sciences ; Metabolism ; Mitogen-Activated Protein Kinase Kinases - metabolism ; NAD ; NADPH Oxidases - metabolism ; Nitrate ; NITRATES ; NITRIC OXIDE ; OXIDATION ; Oxidative Stress ; Peptidyl-dipeptidase A ; PHOSPHORYLATION ; Phosphorylation - drug effects ; PHOSPHOTRANSFERASES ; PLASMA ; Protein Subunits ; Protein Transport ; RATS ; Rats, Wistar ; Receptor, Angiotensin, Type 1 - genetics ; Receptor, Angiotensin, Type 1 - metabolism ; RECEPTORS ; RENIN ; Renin-Angiotensin System - drug effects ; Renin-Angiotensin System - physiology ; Superoxide anion ; superoxide anions ; Superoxides - metabolism ; Toxicology ; TRANSLOCATION
É parte de: Toxicology and applied pharmacology, 2012-11, Vol.264 (3), p.470-478
Notas: ObjectType-Article-2
SourceType-Scholarly Journals-1
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Descrição: Ethanol intake is associated with increase in blood pressure, through unknown mechanisms. We hypothesized that acute ethanol intake enhances vascular oxidative stress and induces vascular dysfunction through renin–angiotensin system (RAS) activation. Ethanol (1g/kg; p.o. gavage) effects were assessed within 30min in male Wistar rats. The transient decrease in blood pressure induced by ethanol was not affected by the previous administration of losartan (10mg/kg; p.o. gavage), a selective AT1 receptor antagonist. Acute ethanol intake increased plasma renin activity (PRA), angiotensin converting enzyme (ACE) activity, plasma angiotensin I (ANG I) and angiotensin II (ANG II) levels. Ethanol induced systemic and vascular oxidative stress, evidenced by increased plasma thiobarbituric acid-reacting substances (TBARS) levels, NAD(P)H oxidase‐mediated vascular generation of superoxide anion and p47phox translocation (cytosol to membrane). These effects were prevented by losartan. Isolated aortas from ethanol-treated rats displayed increased p38MAPK and SAPK/JNK phosphorylation. Losartan inhibited ethanol-induced increase in the phosphorylation of these kinases. Ethanol intake decreased acetylcholine-induced relaxation and increased phenylephrine-induced contraction in endothelium-intact aortas. Ethanol significantly decreased plasma and aortic nitrate levels. These changes in vascular reactivity and in the end product of endogenous nitric oxide metabolism were not affected by losartan. Our study provides novel evidence that acute ethanol intake stimulates RAS activity and induces vascular oxidative stress and redox-signaling activation through AT1-dependent mechanisms. These findings highlight the importance of RAS in acute ethanol-induced oxidative damage. ► Acute ethanol intake stimulates RAS activity and vascular oxidative stress. ► RAS plays a role in acute ethanol-induced oxidative damage via AT1 receptor activation. ► Translocation of p47phox and MAPKs phosphorylation are downstream effectors. ► Acute ethanol consumption increases the risk for acute vascular injury.
Editor: Amsterdam: Elsevier Inc
Idioma: Inglês

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Acute ethanol intake induces superoxide anion generation and mitogen-activated protein kinase phosphorylation in rat aorta: A role for angiotensin type 1 receptor

Yogi, Alvaro ; Callera, Glaucia E. ; Mecawi, André S. ; Batalhão, Marcelo E. ; Carnio, Evelin C. ; Antunes-Rodrigues, José ; Queiroz, Regina H. ; Touyz, Rhian M. ; Tirapelli, Carlos R.

Amsterdam: Elsevier Inc

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