ATP-sensitive and inwardly rectifying potassium channels in smooth muscle

The properties and roles of ATP-sensitive (K(ATP)) and inwardly rectify (K(IR)) potassium channels are reviewed. Potassium channels regulate the membrane potential of smooth muscle, which controls calcium entry through voltage-dependent calcium channels, and thereby contractility through changes in intracellular calcium. The K(ATP) channel is likely to be composed of members of the inward rectifier channel gene family (Kir6) and sulfonylurea receptor proteins. The K(IR) channels do not appear to be as widely distributed as K(ATP) channels in smooth muscle and may provide a mechanism by which changes in extracellular K+ can alter smooth muscle membrane potential, and thereby arterial diameter. The K(ATP) channels contribute to the resting membrane conductance of some types of smooth muscle and can open under situations of metabolic compromise. The K(ATP) channels are targets of a wide variety of vasodilators and constrictors, which act, respectively, through adenosine 3',5'-cyclic monophosphate/protein kinase A and protein kinase C. The K(ATP) channels are also activated by a number of synthetic vasodilators (e.g., diazoxide and pinacidil) and are inhibited by the oral hypoglycemic sulfonylurea drugs (e.g., glibenclamide). Together, K(ATP) and K(IR) channels are important regulators of smooth muscle function and represent important therapeutic targets.