We hypothesized that apocynin (APO), a NOX inhibitor, prevents the development of hypertension and endothelial dysfunction in SHR. SHR was treated from the 4th to 10th week of life with APO (30 mg/Kg/day, in drinking water). At 10th week, MAP, in vivo ACh (2μg/Kg) and phenylephrine (Phe, 8μg/Kg) effects and endothelial cells (EC) reactive oxygen species [ROS] and nitric oxide [NO] concentrations were evaluated. EC were removed from the thoracic aorta and incubated with DHE, a fluorescent dye to ROS, or DAF‐2 DA, to NO. Fluorescence intensity (U) was recorded in EC, before and after acetylcholine (1μmol/L) stimulation. The results (mean±SEM) were compared between SHR+APO, SHR and Wistar (W) rats (ANOVA, p<0.05). MAP was lower in SHR+APO (129.5± 2 mmHg; n=9) than in SHR (160.3± 3). ACh effect was reduced in SHR (−22.2 ± 2 mmHg × W: −31.1± 2), but it was increased in SHR+APO (−40.5 ± 3). Phe effect was increased in SHR+APO (+50.9±1 mmHg × SHR: +42.7±2 × W: +41.8±1). Higher [ROS] was observed in SHR EC (2880.0±0.2U × W: 1822.0±0.1), but it was reduced in SHR+APO (2090.0±0.2). [NO] was increased in SHR+APO (3368.0±0.3 U) and W (3180.0±0.2 × SHR: 2057.0±0.1). ACh increased [NO], and it was higher in SHR+APO (6320.0±0.3 × W: 4526.0±0.3 × SHR:2259.0±0.1U). We demonstrated that the chronic treatment with APO prevented the development of hypertension and endothelial dysfunction in SHR. However, APO increased Phe effect in SHR.