K(+) channels play an essential role in the membrane potential of arterial smooth muscle, and also in regulating contractile tone. Especially, in vascular smooth muscle, the opening of adenosine triphosphate (ATP)-sensitive K(+) (KATP) channels leads to membrane hyperpolarization, resulting in muscle relaxation and vasodilation. This activation also plays a role in tissues during pathophysiologic events such as ischemia, hypoxia, and vasodilatory shock. In this review, we will describe the physiological and pathophysiological roles of vascular smooth muscle KATP channels in relation to the effects of anesthetics. Although accumulated evidence suggests that many anesthetics modify the above function of K(+) channels as a metabolic sensor, further studies are certainly needed to resolve certain issues, especially in clinical settings of anesthesia use.