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.
Henquin
J C
JC
I. Physiologisches Institut, University of Saarland, Homburg/Saar, Federal Republic of Germany.
D000818:Animals; D002118:Calcium / Q000494:pharmacology*; D004594:Electrophysiology; D005260:Female; D005947:Glucose / Q000494:pharmacology*; D007515:Islets of Langerhans / Q000187:drug effects / Q000502:physiology*; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D015221:Potassium Channels / Q000502:physiology*; D012414:Rubidium Radioisotopes / Q000378:metabolism; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000008:administration & dosage / Q000494:pharmacology
D015221:Potassium Channels; D012414:Rubidium Radioisotopes; D013757:Tetraethylammonium Compounds; D019789:Tetraethylammonium; D005947:Glucose; D002118:Calcium