The role of skin temperature in reflex control of the active cutaneous vasodilator system was examined in six subjects during mild graded heat stress imposed by perfusing water at 34, 36, 38, and 40 °C through a tube-lined garment. Skin sympathetic nerve activity (SSNA) was recorded from the peroneal nerve with microneurography. While monitoring esophageal, mean skin, and local skin temperatures, we recorded skin blood flow at bretylium treated and untreated skin sites using laser-Doppler velocimetry and local sweat rate using capacitance hygrometry on the dorsal foot. Cutaneous vascular conductance (CVC) was calculated by dividing skin blood flow by mean arterial pressure. Mild heat stress increased mean skin temperature by 0.2 or 0.3 °C every stage but esophageal and local skin temperature did not change during the first three stages. CVC at the bretylium treated site (CVC_BT) and sweat expulsion number increased at 38 and 40 °C compared to 34 °C (P < 0.05), however CVC at the untreated site did not change. SSNA increased at 40 °C (P < 0.05, different from 34°C). However, SSNA burst amplitude increased (P < 0.05) while SSNA burst duration decreased (P< 0.05) at the same time as we observed the increase in CVC_BT and sweat expulsion number. These data support the hypothesis that the active vasodilator system is activated by changes in mean skin temperature, even at normal core temperature, and illustrates the intricate competition between active vasodilator and the vasoconstrictor system for control of skin blood flow during mild heat stress.