Role of voltage- and Ca2(+)-dependent K+ channels in the control of glucose-induced electrical activity in pancreatic B-cells.

Low concentrations of tetraethylammonium chloride (TEA), which inhibit voltage- and Ca2(+)-sensitive K+ channels (K(+)-VCa channels), were used to investigate whether these channels play a role in the control of glucose-induced electrical activity (slow waves with spikes) in mouse pancreatic B-cells. Addition of 2 mM TEA to a medium containing 0, 3 or 6 mM glucose had no effect on the membrane potential of B-cells or on 86Rb+ efflux and insulin release from isolated islets. In 10 mM glucose, 0.5-2 mM TEA produced a concentration-dependent increase in spike amplitude without modifying slow-wave duration or frequency. Insulin release was only slightly increased under these conditions. In conclusion, K(+)-VCa channels are not operative when the B-cell membrane is not depolarized (in low glucose). They appear to play a role in the repolarization of the spikes but not in that of the slow waves. In contrast to ATP-sensitive K+ channels, K(+)-VCa channels are not a target on which glucose acts to regulate electrical activity in B-cells and, hence, insulin release.