Assessment of the role of angiotensin II in the cardiovascular effects induced by acute ethanol consumption

• Grant number: 10/05815-4
• Support Opportunities: Regular Research Grants
• Start date: April 01, 2011
• End date: September 30, 2013
• Field of knowledge: Biological Sciences - Pharmacology - Cardiorenal Pharmacology
• Principal Investigator: Carlos Renato Tirapelli
• Grantee: Carlos Renato Tirapelli
• Host Institution: Escola de Enfermagem de Ribeirão Preto (EERP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
• Associated researchers: Evelin Capellari Cárnio ; Regina Helena Costa Queiroz

Abstract

Binge drinking has become usual in our society and is defined as the consumption of high doses of ethanol in a short period of time. Acute ethanol intake induces a transient increase in blood pressure. However, the molecular mediators underlying the cardiovascular effects of acute ethanol intake remain elusive. Acute administration of ethanol induces the generation of reactive oxygen species (ROS) in several tissues. In chronically ethanol-treated rats the initial step associated with cardiovascular dysfunction involves increased ROS generation, being this processes mediated by the NADPH oxidase enzyme. Angiotensin II (Ang II) activates NADPH oxidase in the cardiovascular system and both chronic and acute ingestion of ethanol stimulates the rennin-angiotensin system (RAS). A possible role for MAPKs (Mitogen-Activated Protein Kinases) on the effects of ethanol in the cardiovascular system has been described. Ethanol appears to indirectly activate MAPKs in the cardiovascular system. The MAPKs are activated by several stimuli such as ROS and Ang II. The hypothesis of the present study is that acute ethanol intake stimulates RAS which in turn induces the generation of ROS (via NADPH oxidase) and the activation of MAPKs. This process would induce alterations in vascular reactivity and NO bioavailability as well as a transient increase in blood pressure. (AU)

Scientific publications

(6)

(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)

YOGI, ALVARO; CALLERA, GLAUCIA E.; MECAWI, ANDRE S.; BATALHAO, MARCELO E.; CARNIO, EVELIN C.; ANTUNES-RODRIGUES, JOSE; QUEIROZ, REGINA H.; TOUYZ, RHIAN M.; TIRAPELLI, CARLOS R.. Acute ethanol intake induces superoxide anion generation and mitogen-activated protein kinase phosphorylation in rat aorta: A role for angiotensin type 1 receptor. Toxicology and Applied Pharmacology, v. 264, n. 3, p. 470-478, NOV 1 2012. (10/05815-4)

GONZAGA, NATALIA A.; AWATA, WANESSA M. C.; DO VALE, GABRIEL T.; MARCHI, KATIA C.; MUNIZ, JAQUELINE J.; TANUS-SANTOS, JOSE E.; TIRAPELLI, CARLOS R.. Perivascular adipose tissue protects against the vascular dysfunction induced by acute ethanol intake: Role of hydrogen peroxide. VASCULAR PHARMACOLOGY, v. 111, p. 44-53, DEC 2018. (10/05815-4)

CERON, CARLA S.; DO VALE, GABRIEL T.; SIMPLICIO, JANAINA A.; PASSAGLIA, PATRICIA; RICCI, STHEFANY T.; TIRAPELLI, CARLOS R.. Data on the effects of losartan on protein expression, vascular reactivity and antioxidant capacity in the aorta of ethanol-treated rats. DATA IN BRIEF, v. 11, p. 111-116, APR 2017. (10/05815-4)

PASSAGLIA, PATRICIA; CERON, CARLA S.; MECAWI, ANDRE S.; ANTUNES-RODRIGUES, JOSE; COELHO, EDUARDO B.; TIRAPELLI, CARLOS R.. Angiotensin type 1 receptor mediates chronic ethanol consumption-induced hypertension and vascular oxidative stress. VASCULAR PHARMACOLOGY, v. 74, p. 49-59, NOV 2015. (12/10096-2, 10/05815-4)

HIPOLITO, ULISSES V.; CALLERA, GLAUCIA E.; SIMPLICIO, JANAINA A.; DE MARTINIS, BRUNO S.; TOUYZ, RHIAN M.; TIRAPELLI, CARLOS R.. Vitamin C prevents the endothelial dysfunction induced by acute ethanol intake. Life Sciences, v. 141, p. 99-107, NOV 15 2015. (10/05815-4, 10/01383-2)

SIMPLICIO, JANAINA A.; RESSTEL, LEONARDO B.; TIRAPELLI, DANIELA P. C.; D'ORLEANS-JUSTE, PEDRO; TIRAPELLI, CARLOS R.. Contribution of oxidative stress and prostanoids in endothelial dysfunction induced by chronic fluoxetine treatment. VASCULAR PHARMACOLOGY, v. 73, p. 124-137, OCT 2015. (10/05815-4, 13/00808-8)