Objective: Angiotensin II (ang II) activates NAD(P)H oxidase, which is major source of vascular O2- and is associated with elevation of blood pressure (BP) and cardiovascular damage. In the present studies, we used p47phox-deficient mice (p47phox-/-), a cytolic subunit of the NAD(P)H oxidase, to study the role of p47phox in BP elevation and vascular changes induced by ang II-infusion. Method: p47phox-deficient (p47phox-/-) and matched wild-type (C57BL/6; WT) mice were subjected to ang II infusion (0.75 ���/h per day) via mini-osmotic pump in absence and presence of NAD(P)H oxidase inhibitor, apocynin (2.5 mg/day in food) for 7 days (total No=53). Systolic blood pressure (SBP) was measured by tail-cuff method. Structural changes of mesenteric resistance arteries (lumen <200 關m) were evaluated using a pressurized myogroph. Results: Ang II infusion significantly increased SBP from 113짹14 to 157짹7 mm Hg in wild-type mice (p<0.01). In contrast, the hypertensive response to ang II infusion (120짹16 mm Hg) in p47phox-/- mice was markedly blunted (p<0.01). Angiotensin II infusion into WT and p47phox-/- mice induced cardiac hypertrophy. Mesenteric arteries from ang II-infused mice exhibited greater media and media to lumen ratio (12.1짹1.6 關m, 7.3짹0.4 %) than those from WT mice (9.2짹0.4 關m, 6.5짹0.3 %, both p<0.05). However, vascular changes were similar to those of WT mice, in p47phox-/- (10.9짹1.2 關m, 6.9짹0.5%), ang II-infused (10.5짹0.8 關m, 6.7짹0.5 %), and ang II + apocynin-treated p47phox-/- (10.4짹1.3 關m and 6.7짹0.6 %). Conclusion: There results suggest that the deficiency of the NAD(P)H oxidase subunit, p47phox, blunts the elevation of blood pressure and reverses the vascular remodeling induced by angiotensin II infusion.