Abstract
Calcium-/voltage-gated, large-conductance potassium channels (BK) control key physiological processes, including smooth muscle (SM) contraction. Numerous observations concur that elevated membrane cholesterol inhibits homomeric BK consisting of channel-forming alpha subunits. In mammalian SM, however, native BK include accessory beta1 subunits, which increase the channel's apparent calcium sensitivity, favoring activation at physiological intracellular calcium. Thus, BK-driven current negatively feedbacks on depolarization and opposes SM contraction.
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