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Role of NAD (P)H oxidase and perivascular adipose tissue(PVAT) in the vascular effects induced by acute consumption of ethanol

Grant number: 13/20197-3
Support Opportunities:Scholarships in Brazil - Scientific Initiation
Effective date (Start): December 01, 2013
Effective date (End): July 31, 2014
Field of knowledge:Biological Sciences - Pharmacology - Cardiorenal Pharmacology
Principal Investigator:Carlos Renato Tirapelli
Grantee:Gabriela Harumi Teshima
Host Institution: Escola de Enfermagem de Ribeirão Preto (EERP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil


Acute consumption of ethanol induces a transient increase in blood pressure and changes in vascular reactivity. This last response is associated with increased oxidative stress and reduced bioavailability of nitric oxide (NO). The first step for vascular dysfunction associated with the consumption of ethanol involves the formation of reactive oxygen species (ROS) and reduced bioavailability of nitric oxide (NO). The enzyme NAD(P)H oxidase is a major source of ROS in the vasculature. The pathophysiological importance of NAD (P) H oxidase has led many investigators in a large number of experiments both in vivo and in vitro, to the use of inhibitors of this enzyme. Apocynin (APO) is considered the main NAD(P)H inhibitor and it displays a powerful anti-inflammatory and anti-oxidizing in a variety of cell and animal models. The importance of perivascular adipose tissue (PVAT) in modulating vascular function and the mechanisms of the anti contract effects promoted by this tissue have been studied. PVAT express components of the renin-angiotensin system, eNOS enzyme, and NAD(P)H oxidase, which makes it a source of ROS and NO. Together, these elements produced by PVAT participate in the regulation of the functioning and maintenance of vascular tone. However, the participation of the PVAT ethanol-induced vascular alterations has not yet been investigated. The hypothesis of this study is that the acute consumption of ethanol will induce the production of ROS in the vasculature and in PVAT via NAD(P)H oxidase, which will change the modulation of PVAT on vascular response. Therefore, the aim of this study is to evaluate the role of NAD(P)H oxidase, through its inhibition by APO, and PVAT on vascular effects induced by acute consumption of ethanol. (AU)

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