Objective: Oxidative stress seems to be present in all forms of hypertension. An NAD(P)H oxidase is thought to be a main source of vascular free radicals (ROS) production. In this study, we hypothesized that p47phox, NAD(P)H oxidase subunit, contributes blood pressure (BP) elevation and cardio-renal hypertrophy and vascular alterations. Methods: Male p47phox -l- mice and WT (C57BL/6) mice aged 14 weeks and 27 weeks were studied (n=5 each group). SBP measurements were monitored by tail-cuff method. Wet heart (left and right) and kidney were measured to evaluate hypertrophy. To structural (media to lumen ratio) and functional alterations were evaluated in mesenteric arteries using a pressurized myograph. Endothelium-dependent or -independent relaxation was assessed by measuring the dilatory responses to acetylcholine (10-7 to 10-5 mol/L) or sodium nitroprusside (SNP; 10-7 to 10-4 mol/L). Results: At 14 week age, SBP was similar in p47phox -l- mice (107짹5 mm Hg), compared with control mice (113짹6 mm Hg). Relative cardiac and renal weights were lower in p47phox -l- mice. Structural changes (media to lumen ratio) in mesenteric artery were similar in p47phox -l- mice (5.9짹0.2 %) compared with control mice (6.0짹0.3 %). Vasodilatory responses to a maximal dose of acetylcholine or sodium nitroprusside were similar in both groups (about 93 and 98%). At 27 week, SBP elevation was blunted in p47phox -l- mice (vs. WT mice). In p47phox -l- mice aged of 27 week, relative cardiac and renal hypertrophy and BP elevation was decreased or blunted compared to those of 14-week p47phox -l- mice. Conclusions: p47phox, NAD(P)H oxidase subunit, may contribute BP elevation and cardio-renal hypertrophy, which were demonstrated in p47phox -l- mice. Even though structural changes were similar between middle-aged p47phox -l- and WT mice, it needs to be determined in old-aged mice.