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.
D000818:Animals; D002463:Cell Membrane Permeability; D002712:Chlorides / Q000378:metabolism*; D005260:Female; D005947:Glucose / Q000494:pharmacology; D007473:Ion Channels / Q000187:drug effects / Q000378:metabolism; D007515:Islets of Langerhans / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D008820:Mice, Obese
D002712:Chlorides; D007473:Ion Channels; D005947:Glucose