Full expression of reflex cutaneous vasodilation (VD) is dependent on nitric oxide (NO), and is attenuated with essential hypertension (HTN). Decreased NO-dependent VD may be due to 1) increased oxidant stress and/or 2) decreased L-arginine availability through upregulated arginase activity, potentially leading to increased superoxide production through uncoupled NO-synthase (NOS). The purpose of this study was to determine the effect of antioxidant supplementation and arginase inhibition on attenuated NO-dependent reflex cutaneous VD in hypertensive subjects. Nine unmedicated hypertensive (HT: MAP=112±1mmHg) and 9 age-matched normotensive (NT: MAP=81±10) men and women were instrumented with 4 intradermal microdialysis (MD) fibers: control (Co), NOS inhibited (NOS-I: L-NAME), L-ascorbate (Asc: L-ascorbate), and Asc+arginase-inhibited (Asc+A-I: L-ascorbate+BEC+nor-NOHA). Oral temperature (T_or) was increased by 0.8°C via a water-perfused suit. L-NAME was then ultimately perfused through all MD sites to quantify the change in VD due to NO. Red blood cell flux was measured using laser-Doppler over each skin MD site, and cutaneous vascular conductance (CVC) was calculated and normalized to maximal CVC (28mM sodium nitroprusside + local heating to 43°C). During the plateau in skin blood flow (T_or=0.8°C ), cutaneous VD was attenuated in HT skin (NT: 42±4, HT: 35±3%CVC_max, p<0.05). Asc and Asc+A-I augmented cutaneous VD in HT (Asc: 57±5, Asc+A-I: 53±6%CVC_max, p<0.05 vs. Co), but not NT. %CVC_max after NOS-I in the Asc and Asc +A-I sites was increased in HT (Asc: 41±4, Asc+A-I: 40±4 vs. Co: 29±4%CVC_max; both p<0.05). Compared to the Co site, the change in %CVC_max within each site after NOS-I was greater in HT (Asc: -19±4, Asc+A-I: -17±4 vs. Co: -9±2%CVC_max, p<0.05) but not NT. Ascorbate alone or combined with arginase inhibition augments attenuated reflex cutaneous VD in HTN skin through NO- and non-NO-dependent mechanisms.