Cholesterol depletion alters amplitude and pharmacology of vascular calcium-activated chloride channels

摘要

AimsCalcium-activated chloride channels (CACCs) share common pharmacological properties with Kcnma1-encoded large conductance K⁺ channels (BKCa or KCa1.1) and it has been suggested that they may co-exist in a macromolecular complex. As KCa1.1 channels are known to localize to cholesterol and caveolin-rich lipid rafts (caveolae), the present study investigated whether Ca²⁺-sensitive Cl⁻ currents in vascular myocytes were affected by the cholesterol depleting agent methyl-β-cyclodextrin (M-βCD).