Halothane is a popular inhalation anesthetics in practice, which has been reported to cause a vasodilation through a direct depressant action on vascular smooth muscle, or by an indirect attenuation of vasoconstrictor activity. The membrane potential of the vascular smooth muscle cell is mainly regulated by the flow of Ca2+ and K+ ions through specialized channels. The purpose of this study was to determine whether blockade of the K+ channel alter the response to halothane vasodilating action. This study was done with rat thoracic aorta in tissue bath. Isometric tension of the ring (3~4 mm in length) was recorded. In halothane alone group (n=15), after precontraction with norepinephrine (10(-7) M), ring was exposed with halothane 0.7%, 1.5%, 2.1% concentration for 15 minutes, sequentially. The procedure of calcium activated K+ channel blocker pretreated group (n=12) was same manner as halothane alone group after tetraethylammonium (TEA 20 mM) pretreatment. The result of this study was shown to followings; 1) Vasodilation correlate with halothane concentration (p<0.05). 2) Vasodilation in tetraethylammonium (TEA) pretreated group also augmented 'significantly (p<0.05). 3) Especially, in the halothane 1.5%, 2.1%, the presence of TEA significantly potentiate vasodilating effect: halothane alone group, -35%, -53%: TEA group, -47%, -71%(p<0.05). These result demonstrate that: 1) halothane induce relaxation of rat aorta. 2) K+ charinel blokade potentiate the vasodilating effect of halothane.