Acetylcholine released from cholinergic nerves is involved in heat loss responses of cutaneous vasodilation and sweating. K⁺ channels are thought to play a role in regulating cholinergic cutaneous vasodilation and sweating, though which K⁺ channels are involved in their regulation remains unclear. We evaluated the hypotheses that 1) Ca²⁺-activated K⁺ (K_Ca), ATP-sensitive K⁺ (K_ATP), and voltage-gated K⁺ (K_V) channels all contribute to cholinergic cutaneous vasodilation; and 2) K_V channels, but not K_Ca and K_ATP channels, contribute to cholinergic sweating. In 13 young adults (24±5 years), cutaneous vascular conductance (CVC) and sweat rate were evaluated at intradermal microdialysis sites that were continuously perfused with: 1) lactated Ringer (Control), 2) 50mM tetraethylammonium (K_Ca channel blocker), 3) 5mM glybenclamide (K_ATP channel blocker), and 4) 10mM 4-aminopyridine (K_V channel blocker). At all sites, cholinergic cutaneous vasodilation and sweating were induced by co-administration of methacholine (0.0125, 0.25, 5, 100, and 2000mM, each for 25 min). The methacholine-induced increase in CVC was lower with the K_Ca channel blocker relative to Control at 0.0125 (1±1 vs. 9±6%max) and 5 (2±5 vs. 17±14%max) mM methacholine, whereas it was lower in the presence of K_ATP (69±7%max) and K_V (57±14%max) channel blocker in comparison to Control (79±6%max) at 100mM methacholine. Further, methacholine-induced sweating was lower at the K_V channel blocker site (0.42±0.17mg•min^-1•cm^-2) compared to Control (0.58±0.15mg•min^-1•cm^-2) at 2000mM methacholine. In conclusion, we show that K_Ca, K_ATP, and K_V channels play a role in cholinergic cutaneous vasodilation, whereas only K_V channels contribute to cholinergic sweating in normothermic resting humans.