Plasma hyperosmolality delays the response in skin blood flow and sweating to heat stress by elevating the internal temperature threshold for cutaneous vasodilation. This elevation could be due to a delayed onset of cutaneous active vasodilation and/or to persistent cutaneous active vasoconstriction. Seven healthy men were infused with either hypertonic (3% NaCl) or isotonic (0.9 % NaCl) saline and passively heated by immersing their lower legs in 42 °C water for 60 min (room temperature, 28°C; RH, 40 %). Skin blood flow was monitored via laser-Doppler flowmetry at sites pretreated with bretylium tosylate (BT) to block sympathetic vasoconstriction selectively and at adjacent control sites. Plasma osmolality was increased by ~13 mOsm/kg H₂O following hypertonic saline infusion, and was unchanged following isotonic saline infusion. The esophageal temperature (T_es) threshold for cutaneous vasodilation at untreated sites was significantly elevated in the hyperosmotic state (37.73±0.11°C) relative to the isosmotic state (36.63±0.12°C, P<0.001). A similar elevation of the T_es threshold for cutaneous vasodilation was observed between osmotic conditions at the BT-treated sites (37.74±0.18 vs. 36.67±0.07°C, P<0.001) as well as sweating. These results suggest that the hyperosmotically-induced elevation of the internal temperature threshold for cutaneous vasodilation is due primarily to an elevation in the internal temperature threshold for the onset of active vasodilation, and not to an enhancement of vasoconstrictor activity.