Reflex cutaneous vasodilatation is dependent on nitric oxide (NO), which is diminished in hypertension (HTN). Arginase may be upregulated with HTN, which preferentially metabolizes L-arginine (L-arg), competing with NO-synthase-mediated pathways and limiting NO synthesis. We hypothesized that NO-dependent vasodilatation would be attenuated in HTN skin, and arginase inhibition (A-I) alone or with concurrent L-arginine supplementation, would augment vasodilatation. Five microdialysis fibres were placed in skin of 8 unmedicated subjects with HTN (MAP: 112±1 mmHg) and 9 age-matched normotensive (AMN) (MAP: 87±1 mmHg) men and women to serve as: control (C: Ringers), NOS inhibited (NOS-I: 10mM L-NAME), A-I (5mM BEC + 5mM nor-NOHA), L-arg supplemented (L-arg: 10mM L-arg), and combined A-I + L-arg. Reflex vasodilatation was induced by using a water-perfused suit to increase oral temperature (Tor) 1.0°C. Red cell flux was measured by laser-Doppler over each site. Cutaneous vascular conductance was calculated (CVC=flux/MAP) and normalized to maximal CVC (28mM SNP + local heating to 43°C). The Ä%CVCmax between the control and NOS-I site was calculated as the difference between Co and NOS-I sites. Maximal CVC was attenuated in the HTN subjects by ~25% compared to AMN subjects (p<0.001). Throughout whole body heating %CVCmax was not different between the groups (HTN: 43±3 vs. AMN: 45±3%CVCmax, p>0.05). NOS-I significantly decreased %CVCmax in both groups but %CVCmax was greater in the HTN group (HTN: 32±4 vs. AMN: 23±3%CVCmax, p<0.05). The Ä%CVCmax between the control and NOS-I sites was attenuated at ÄTor>0.5°C in the HTN group (p<0.001 vs. AMN). A-I alone augmented %CVCmax only in the HTN group (HTN: 65±5 vs. AMN: 48±3%CVCmax, p<0.05). L-arg alone did not affect %CVCmax in either group (HTN: 49±5 vs. AMN: 49±3%CVCmax, p>0.05). Combined A-I+L-arg augmented %CVCmax in both subject groups compared to their respective control sites (HTN: 60±7 vs. AMN: 61±3%CVCmax, both p<0.05 vs. respective control sites). Vasodilatation is attenuated with HTN due to decreased NO-dependent vasodilation and can be augmented with arginase inhibition but not L-arg supplementation, suggesting that arginase is upregulated with HTN.