CALCIUM-DEPENDENT REGULATION OF MEMBRANE ION PERMEABILITY IN A CELL-LINE DERIVED FROM THE EQUINE SWEAT GLAND EPITHELIUM

We measured the rates of I-125(-) and Rb-86(+) efflux from preloaded, cultured equine sweat gland cells. The calcium ionophore ionomycin inc reased the efflux of both isotopes, Anion efflux was unaffected by Ba2 +, but this cation inhibited Rb-86(+)-efflux, suggesting that [Ca2+](i )-activated potassium channels were present. Activation of these chann els was not, however, important for the efflux of anions. We measured I-125(-) efflux from valinomycin-depolarised cells in which anion cotr ansport was inhibited. Changes in I-125(-) efflux reflect changes in a nion permeability under these conditions, and ionomycin caused a clear permeability increase that was abolished by the anion channel blocker diphenylamine-2-carboxylate. ATP and UTP increased the efflux of both isotopes, suggesting that type P-2U purine receptors allow these nucl eotides to regulate membrane permeability.