Hyperandrogenism and vascular dysfunction often coexist in women with Polycystic Ovary Syndrome (PCOS). We hypothesized that testosterone compromises cutaneous microvascular dilation in women with PCOS via the endothelin-1 ET-B subtype receptor. To control and isolate testosterone effects on microvascular dilation, we administered a gonadotropin releasing hormone antagonist (GnRHant) for 11 days in obese otherwise healthy women [(Controls, 22.0 (4) y, 36.0 (3.2) kg/m²)] or women with PCOS [23 (4) y, 35.4 (1.3) kg/m2)], adding testosterone (T, 2.5 mg/day) for days 8-11. Using laser Doppler flowmetry and cutaneous microdialysis, we measured changes in skin microcirculatory responsiveness (CVC) to local heating while perfusing ET-A (BQ-123) and ET-B (BQ-788) receptor antagonists under three experimental conditions: baseline (BL, pre-hormone intervention), GnRHant (day 4 of administration), and T administration. At BL, ET-A receptor inhibition enhanced heat-induced vasodilation in both groups [CVC Control 2.03 (0.65), PCOS 2.10 (0.25), AU/mmHg, P< 0.05]; ET-B receptor inhibition reduced vasodilation in Controls only [CVC 0.98 (0.39), 1.41 (0.45) AU/mmHg for Controls, PCOS] compared to saline [CVC Controls 1.27 (0.48), PCOS 1.31 (0.13) AU/mmHg]. GnRHant enhanced vasodilation in PCOS [saline CVC 1.69 (0.23) AU/mmHg vs. BL, P<0.05), and abolished the ET-A effect in both groups; a response reasserted with T in Controls. ET-B receptor inhibition reduced heat-induced vasodilation in both groups during GnRHant and T [CVC, Controls: 0.95 (0.21) vs. 0.51 (13), PCOS: 1.27 (0.23) vs. 0.84 (0.27); for GnRHant vs. T, P< 0.05)]. These data demonstrate androgen suppression improves microvascular dilation in PCOS via ET-A and ET-B receptors.