The role of vascular NAD(P)H oxidase in subarachnoid hemorrhage (SAH)-induced vasospasm in the basilar artery was examined in a rat model. Arterial vasospasm characterized by increased wall thickness and decreased lumen size was observed at 5 to 7 days after 2nd injection of blood into cisterna magna, and these changes were significantly ameliorated by pretreatment of diphenyleneiodonium (DPI, 25μl of 100μM), an inhibitor of NAD(P)H oxidase. To determine the time course of changes in the vascular NAD(P)H oxidase activity, cerebral vasculature was isolated at different time intervals from 12 hrs to 14 days after injection of autologous blood. At 24 hrs after the second injection of blood, the NAD(P)H oxidase activity was markedly increased with an enhanced membrane translocation of p47phox, but by 48 hours both the enzyme activity and p47phox translocation regained normal values, and were remained unchanged up to 14 days after SAH. However, no significant changes in the expression of p22phox mRNA was observed throughout the experiments. These findings suggest that the activation of NAD(P)H oxidase by which assembly of the oxidase components enhanced and subsequent production of superoxide in the early stages of SAH might contribute to the delayed cerebral vasospasm in SAH rats.