1. Regulation of smooth muscle membrane potential through changes in K
+ channel activity and subsequent alterations in the activity of volta
ge-dependent calcium channels is a major mechanism of vasodilation and
vasoconstriction, both in normal and pathophysiological conditions. T
he contribution of a given K+ channel type to this mechanism of vascul
ar regulation depends on the vascular bed and species examined. 2. Mul
tiple 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+ (K-v) channels are activated by depolarizat
ion, may contribute to steady state resting membrane potential and are
inhibited by certain vasoconstrictors. Calcium-activated K+ (K-Ca) ch
annels oppose the depolarization associated with intrinsic vascular to
ne and are activated by some endogenous vasodilators. Small-conductanc
e, apamin-sensitive K-Ca channels may be activated by endothelium-deri
ved hyperpolarizing factor. ATP-sensitive K+ (K-ATP) channels are acti
vated 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 potent
ial and diameter are determined, in part, by the integrated activity o
f several K+ channels, which are regulated by multiple dilator and con
strictor signals in vascular smooth muscle.