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 Ca
2+ concentration and membrane depolarization stimulate large-conductance Ca
2+-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.
View full abstract