It is known that renal oxidative stress reflects an imbalance between increased generation of oxidants and attenuated antioxidant defense systems and it has been demonstrated that it plays an important role in arterial hypertension. In hypertension, elevated levels of angiotensin II (Ang II) activates NAD(P)H oxidases via interaction with Ang II type 1 (AT-1) receptors thereby producing oxidative stress. Previous studies in our laboratory have shown that this mechanism occurs in premotor regions of the sympathetic nervous system in renovascular hypertensive rats, contributing to sympathoexcitation, mainly renal, and maintenance of hypertension. The hypothesis of this project is that the increased activity of the renal nerves contributes to oxidative stress in the kidneys of renovascular hypertensive rats (2 Kidney - 1 Clip model). For that, renal denervation will be performed and subsequent evaluation of renal oxidative stress by dihydroethidium (DHE) fluorescence analysis which evaluates the production of reactive oxygen species (ROS) in tissue and by gene quantification of NAD(P) H oxidase subunits (p47phox and gp91phox) and antioxidant enzymes (catalase, glutathione peroxidase and superoxide dismutase) by real time PCR. Since oxidative stress may contribute to the disorder of renal function, it will be analyzed urinary volume, excretion of sodium (Na +) and proteinuria after denervation.
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