Preeclampsia (PE) is a multisystem disorder of pregnancy characterized by hypertension, proteinuria and edema. PE is associated with endothelial dysfunction, oxidative stress and decreased endothelial nitric oxide synthase activity. The mechanisms of normal pregnancy-associated vasodilatation suggest that nitric oxide (NO) is the most important mediator for the reduction of vascular resistance. Inhibition of NO synthesis with L-NAME in pregnant rats is known to result in an animal model of PE-like syndrome with hypertension, proteinuria, thrombocytopenia and intrauterine growth retardation. We assessed the possible relation between oxidative stress and renal dysfunction in this animal model of preeclampsia, by determining the effect of tempol and apocynin on the activity of three antioxidant enzymes: catalase, superoxide dismutase and glutathione peroxidase in the rat kidney. Experiments were performed on 12-13 week primigravida female Sprague-Dawley rats. At day 13 of pregnancy, animals were randomly distributed into the following groups receiving treatment during 7 days: CONTROL: vehicle (NaCl 0.9%); L-NAME: (50 mg/kg/day); TEMPOL: (20mg/kg/day), L-NAME+TEMPOL; APO: (33 μg/kg/day) and L-NAME+APO. Cardiovascular parameters were determined using a tail-cuff digital plethysmograph. Renal cortical antioxidant enzyme activity was determined spectrophotometrically. Chronic administration of L-NAME in pregnant rats increased MAP (+20 mmHg), produced proteinuria and reduced fetuses weight. Likewise, inhibition of NO synthesis decreased CAT, SOD, GPx activity in renal cortical tissue. Tempol or apocynin treatment attenuated hypertension, proteinuria, and reduction in fetus resorption and blunted the reduction of enzyme activity induced by L-NAME in pregnant rats. These findings suggest that reactive oxygen species play an important role in mediating hypertension and renal dysfunction in response to chronic NOS inhibition in pregnant rats.