Abstract

Calcium- and voltage-gated K+ channels of big conductance (BK) regulate cerebral artery smooth muscle (SM) contraction. BK complexes include tissue-specific accessory subunits (beta1-4, encoded by KCNMB1-4) that embolden BK currents with distinct kinetic and pharmacological phenotypes. Beta1 is predominant in SM where it increases the BK’s apparent calcium sensitivity. Moreover, while cholesterol (CLR) inhibits homomeric BK made of channel-forming alpha subunits, beta1 subunit-including BKs are activated by this sterol via up-regulation of beta1 levels in the plasma membrane of cerebral artery SM cells.

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