Skin-surface cooling elicits a pronounced systemic pressor response, which has previously been reported to be associated with peripheral vasoconstriction and may not fully account for the decrease in systemic vascular conductance. To test the hypothesis that whole-body skin-surface cooling would also induce renal and splanchnic vasoconstriction, 14 supine subjects performed 26 skin-surface cooling trials (15-18°C water perfused through a tube-lined suit for 20 min). Oral and mean skin temperature, heart rate, stroke volume (Doppler ultrasound), mean arterial pressure (MAP), cutaneous blood velocity (laser Doppler), and mean blood velocity of the brachial, celiac, renal, and superior mesenteric arteries (Doppler ultrasound) were measured during normothermia and skin-surface cooling. Cardiac output (heart rate·stroke volume) and indexes of vascular conductance (blood velocity/MAP) were calculated. Skin-surface cooling increased MAP (n=26; 78±5 to 88±5 mmHg; mean±SD) and decreased mean skin temperature (n=26; 33.7±0.7 to 27.5±1.2°C) and cutaneous (n=12; 0.93±0.68 to 0.36±0.20 flux mmHg-1), brachial (n=10; 32±15 to 20±12), celiac (n=8; 85±22 to 73±22), superior mesenteric (n=8; 55±16 to 48±10), and renal (n=8; 74±26 to 64±20 cm sec^-1 mmHg^-1; all P<0.05) vascular conductance, without altering oral temperature, cardiac output, heart rate, or stroke volume. These data identify decreases in vascular conductance of skin and of brachial, celiac, superior mesenteric, and renal arteries. Thus, it appears that vasoconstriction in both peripheral and visceral arteries contributes importantly to the pressor response produced during skin-surface cooling in humans.