The chronic ethanol consumption may be associated with many cardiovascular diseases such as hypertension. However, little is known about the molecular mediators associated with cardiovascular effects induced by chronic ethanol intake. Studies suggested that endothelial dysfunction is a potential mechanism responsible for the increase in blood pressure associated with ethanol consumption and the formation of ROS derived from NAD(P)H oxidase lead to vascular endothelial dysfunction. The O2- from the NAD(P)H oxidase is the main ROS in the cardiovascular system. The O2- is able of reacting with nitric oxide (NO) and to form peroxynitrite (OONO-), resulting in protein nitrotyrosylation. The O2- is able of activating NF-ºB in addition to inducing the expression of cyclooxygenase 2 (COX-2) and iNOS which are important mediators of the vascular inflammation. Moreover the ROS produced by NAD(P)H oxidase act as signaling molecules and activate intracellular pathways such as MAPKs (Mitogen-Activated Protein Kinases) that play an important role in intracellular signaling and vascular pathophysiology.The most important NAD(P)H oxidase inhibitor is apocynin. its effect results from blockage of translocation subunit p47phox to the membrane, thus preventing the activation of the enzyme. The apocynin was effective in cardiovascular disease like hypertension. With respect to ethanol, treatment with apocynin prevented cardiac and hepatic necrosis induced by ethanol, suggesting the involvement of NAD(P)H in this response. Despite the importance of ROS in the pathophysiology of ethanol on the cardiovascular system, there are no reports on the participation of NAD(P)H in the process. The aim of this study is to evaluate the involvement of NAD(P)H in vascular dysfunction induced by chronic ethanol consumption in resistance arteries. It is also proposed to evaluate the participation of redox signaling in vascular inflammation induced by ethanol.
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