Oxidative stress is associated with vascular dysfunction in several conditions. Acute exposure to hypoxia also results in reduced vascular function, which has been attributed to increases in hypoxemic-induced elevations in sympathetic nerve activity and oxidative stress. Although the former mechanism has been investigated, it has yet to be determined whether there is a direct link between hypoxia-induced oxidative stress and microvascular dysfunction. We tested the hypothesis that cutaneous vasodilation is impaired by reactive oxygen species from NADPH oxidase and xanthine oxidase pathways. The contribution of nitric oxide (NO) to vasodilation was also quantified. Four intradermal microdialysis membranes were inserted in the forearms of six male participants [age: 25 (3) years; BMI: 24.2 (2.2) kg/m2] on two separate days of either normobaric normoxia (NORM) or normobaric hypoxia (FIO2=0.13; HYP). The order of the days were counterbalanced between participants. The four sites were infused with 1) lactated Ringer solution (control), 2) 100 µM Apocynin (NADPH oxidase inhibitor), 3) 10 µM Tempol (superoxide scavenger), and 4) 10 µM Allopurinol (xanthine oxidase inhibitor). Skin blood flux was measured at each site with laser-Doppler flowmetry continually during the baseline, 39°C local heating, 20 mM L-NAME infusion, and 44°C local heating combined with 28 mM sodium nitroprusside infusion to achieve maximal vasodilation. Data are presented as cutaneous vascular conductance (CVC; flux/mean arterial pressure) as a percentage of maximal values (%CVCmax). During 39°C heating, there was no difference in vasodilation between conditions at the control site [NORM: 68 (16)% vs. HYP: 68 (17)%] and the contribution of NO-dependence was also similar in each condition [NORM: 45 (13)% vs. HYP: 49 (9)%]. There was no significant interaction (two-way ANOVA) between condition and any drug at 39°C heating (P=0.34) or during L-NAME infusion (P=0.38). Therefore, our preliminary data indicate that, at least in acute normobaric hypoxia, oxidative stress does not impair cutaneous vasodilation or its NO-mediated contribution.