The potassium permeability of pancreatic islet cells: mechanisms of control and influence on insulin release.

The K+ permeability of pancreatic islet cells was evaluated by monitoring the efflux of 42K+ or 86Rb+ and measuring the uptake of 42K+ in rat islets. Glucose rapidly and reversibly reduces 42K+ (or 86Rb+) efflux without apparent effect on the rate of 42K+ uptake. This decrease in passive K+ permeability is not secondary to insulin release as it does not require extracellular Ca, and is most marked for changes in the glucose concentration between 3 and 6 mM. This property of glucose is shared by all metabolized sugars, but by none of the nonmetabolized sugars tested. Inhibition of glucose metabolism by islet cells prevents the sugar from decreasing their K+ permeability. Reduction of the redox couple NAD(P)H/NAD(P) appears to be an important link between glucose metabolism and the K+ system in the membrane. A pharmacological decrease of the potassium permeability in islet cells (by tetraethylammonium or 9 aminoacridine) potentiates (and to some extent even mimicks) the insulin-releasing property of glucose. A pharmacological increase (by valinomycin) of this permeability inhibits glucose-stimulated insulin release. The results clearly establish the importance of the decrease in the K+ permeability of B-cell membranes for the physiological response to the stimulation by glucose.