Potassium channels in vascular smooth muscle

Abstract

1. Regulation of smooth muscle membrane potential through changes in K+ channel activity and subsequent alterations in the activity of voltage-dependent calcium channels is a major mechanism of vasodilation and vasoconstriction, both in normal and pathophysiological conditions. The contribution of a given K+ channel type to this mechanism of vascular regulation depends on the vascular bed and species examined. 2. Multiple K+ channels are present in most vascular smooth muscle cells and these different K+ channels play unique roles in regulating vascular tone. Voltage-dependent K+ (Kv) channels are activated by depolarization, may contribute to steady state resting membrane potential and are inhibited by certain vasoconstrictors. Calcium-activated K+ (K(Ca)) channels oppose the depolarization associated with intrinsic vascular tone and are activated by some endogenous vasodilators. Small-conductance, apamin-sensitive K(Ca) channels may be activated by endothelium-derived hyperpolarizing factor. ATP-sensitive K+ (K(ATP)) channels are activated by pharmacological and endogenous vasodilators. Inward rectifier K+ (K(ir)) channels are activated by slight changes in extracellular K+ and may contribute to resting membrane potential. 3. Membrane potential and diameter are determined, in part, by the integrated activity of several K+ channels, which are regulated by multiple dilator and constrictor signals in vascular smooth muscle.