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

ABSTRACT:

Aims

Calcium-activated chloride channels (CACCs) share common pharmacological properties with Kcnma1-encoded large conductance K(+) channels (BK(Ca) or K(Ca)1.1) and it has been suggested that they may co-exist in a macromolecular complex. As K(Ca)1.1 channels are known to localize to cholesterol and caveolin-rich lipid rafts (caveolae), the present study investigated whether Ca(2+)-sensitive Cl(-) currents in vascular myocytes were affected by the cholesterol depleting agent methyl-beta-cyclodextrin (M-betaCD).

Methods and results

Calcium-activated chloride and potassium currents were recorded from single murine portal vein myocytes in whole cell voltage clamp. Western blot was undertaken following sucrose gradient ultracentrifugation using protein lysates from whole portal

SUBMITTER: Sones WR 

PROVIDER: S-EPMC2904657 | biostudies-literature | 2010 Aug

REPOSITORIES: biostudies-literature