The vascular endothelium plays important role on the tone control due to the release of contractile factors (EDCFs) as well relaxant factors from endothelial cells (EDRFs). In some cardiovascular diseases such as hypertension the mechanisms of balance between EDCFs and EDRFs are impaired with augmented levels of reactive oxygen species (ROS). ROS can alter the signaling, production and/or bioavaialbility of nitric oxide (NO), the main EDRF, and to increase the concentrations of prostanoids like prostaglandins (PGs) and thromboxane (TXs), major EDCFs. Renal hypertensive rats 2 kidney-one clip (2K-1C) present augmented levels of angiotensin II (Ang II) that activates AT1 receptors and produce ROS like O2- and H2O2, activation of the enzyme NADH/NADPH oxidase, the main pathway involved on ROS production in the endothelial cells. Compounds that can act as NO donor and cyclooxigenase (COX) inhibitor such as NCX2121, can be used as pharmacological approach. Therefore, the present study aims to characterize the relaxation induced by the compound NCX2121 in 2K-1C rat aorta and to investigate the role of ROS formed in the endothelial cells and the endogenous prostanoids. In this study we will investigate the vascular reactivity to NCX2121. The measurement of NO concentrations will be done by confocal microscopy, ROS in the endothelial cells will be quantified by flow citometry, and the levels of TXA2 and PGI2 stimulated by NCX 2121 will be measured by Elisa-Imuno-assay.
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