Abstract
ATP-sensitive potassium (KATP) channels are inhibited by intracellular ATP and activated by MgADP and thus provide a link between the cellular metabolic state and excitability. KATP (VSM KATP channels) are composed of an ATP-binding cassette protein family, sulfonylurea receptor 2B, and an inward rectifying K+ channel subunit, Kir6.1. SUR2B that acts as a regulatory subunit while Kir6.1 subunits form the channel pore. Recent molecular biological and molecular genetic studies of VSM KATP channels have provided insights into the structure-function relationships, molecular regulation, and pathophysiological roles of KATP channels. VSM KATP channels respond to changes in cellular metabolism and play important roles in the vascular responses to a variety of pharmacological and endogenous vasodilators. In addition, studies performed in Kir6.1 or SUR2B knockout mice indicate that VSM KATP channels are involved in the regulation of vascular tonus, especially in the coronary arteries, and disruption of them may cause Prinzmetal angina. Recent studies also suggest that some anesthetics may influence VSM KATP channels activities. The coronary vasodilatory effects of volatile anesthetics are mediated by activation of VSM KATP channels. In contrast, most intravenous anesthetics and local anesthetics inhibit VSM KATP channels.
