In this review, we present the basic properties, physiological functions, regulation, and pathological alterations of four major classes of K⁺ channels that have been detected in vascular smooth muscle cells. Voltage-dependent K⁺ (Kv) channels open upon depolarization of the plasma membrane in vascular smooth muscle cells. The subsequent efflux of K⁺ through the channels induces repolarization to the resting membrane potential. Changes in the intracellular Ca²⁺ concentration and membrane depolarization stimulate large-conductance Ca²⁺-activated K⁺ (BK_Ca) channels, which are thought to play an important role in maintaining the membrane potential. ATP-sensitive K⁺ (K_ATP) channels underscore the functional bond between cellular metabolism and membrane excitability. The blockade of K_ATP channel function results in vasoconstriction and depolarization in various types of vascular smooth muscle. Inward rectifier K⁺ (Kir) channels, which are expressed in smooth muscle of the small-diameter arteries, contribute to the resting membrane potential and basal tone. Kir channel activation has been shown to raise the extracellular K⁺ concentration to 10-15 mM, resulting in vasodilation. Each of K⁺ channels listed above is responsive to a number of vasoconstrictors and vasodilators, which act through protein kinase C (PKC) and protein kinase A (PKA), respectively. Impaired Kv, K_ATP, and Kir channel functions has been linked to a number of pathological conditions, which may lead to vasoconstriction.