Evidence for voltage-dependent C1- permeability in mouse pancreatic beta-cells.

Microdissected beta-cell-rich pancreatic islets from ob/ob-mice were used in studies of transmembrane 36Cl- efflux. The mean rate coefficient for 36Cl- efflux was stable at 0.158 min-1 during the initial 10 min. Depolarization of the beta-cell plasma membrane by acute increases in extracellular K+ (5-130 mM) stimulated the 36Cl- efflux in a concentration-dependent manner. Glucose-induced (20 mM) and K+-induced increases in 36Cl- efflux were largely overlapping, but even at 135.9 mM K+, glucose slightly further enhanced the 36Cl- efflux rate. The data suggest that pancreatic beta-cells are equipped with a voltage-dependent Cl- permeability, that glucose-induced increase in Cl- permeability may, at least partly, be mediated by primary membrane depolarization, and that glucose in addition may activate other mechanisms for beta-cell Cl- transport.