The vasodilation response to local cutaneous heating is nitric oxide (NO) dependent, blunted in postural tachycardia (POTS) but reversed by angiotensin-II type-1 receptor (AT1R) blockade. We tested the hypothesis that localized infusion of angiotensin-II attenuates vasodilation to local heating in healthy volunteers. We heated skin of the calf to 42°C and measured local blood flow to assess conductance (%CVCmax) in 8 healthy volunteers aged 19.5-25.5 years. Initially, two experiments were performed: in one, Ringer solution was perfused in 3 catheters, the response to heating measured, 2µg/L losartan, 10mM NLA, or NLA+losartan were added to perfusate, and the heat response was remeasured; in another 10µM Ang-II was given, the heat response measured, losartan, NLA, or NLA+losartan were added to Ang-II, and the heat response reassessed. The heat response decreased with angiotensin-II, particularly the plateau phase (47±5 vs 84±3 %CVCmax). Losartan increased baseline conductance in both experiments (from 8±1 to 20±2 and 12±1 to 24±3). Losartan increased Ang-II response (83±4 vs 91±6 in Ringer). NLA decreased both angiotensin and Ringer responses (31±4 vs 43±3,). NLA+losartan blunted the Ringer response (48±2), but the Ang-II response (74±5) increased. In a second set of experiments we used dose-responses to Ang-II (0.1nM to 10µM) with and without NLA+losartan to confirm graded responses. Sodium ascorbate (10mM) restored the Ang-II blunted heating plateau. NOS and AT1R inhibition cause an NO-independent angiotensin-mediated vasodilation with local heating. Angiotensin-II mediates AT1R blunting of local heating which is not exclusively NO dependent, and is improved by antioxidant supplementation.