Cholesterol activates BK channels by increasing KCNMB1 protein levels in the plasmalemma.

ABSTRACT: Calcium-/voltage-gated, large-conductance potassium channels (BKs) control critical physiological processes, including smooth muscle contraction. Numerous observations concur that elevated membrane cholesterol (CLR) inhibits the activity of homomeric BKs consisting of channel-forming alpha subunits. In mammalian smooth muscle, however, native BKs include accessory KCNMB1 (β₁) subunits, which enable BK activation at physiological intracellular calcium. Here, we studied the effect of CLR enrichment on BK currents from rat cerebral artery myocytes. Using inside-out patches from middle cerebral artery (MCA) myocytes at [Ca²⁺]_free=30 μM, we detected BK activation in response to in vivo and in vitro CLR enrichment of myocytes. While a significant increase in myoc

SUBMITTER: Bukiya AN 

PROVIDER: S-EPMC7950327 | biostudies-literature | 2021 Jan-Jun

REPOSITORIES: biostudies-literature