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We have monitored whole-cell and single channel ATP-sensitive K+ (KATP) currents in isolated rat glucagon-secreting pancreatic A-cells. Tolbutamide produced a concentration-dependent decrease in the whole-cell KATP conductance (Ki = 6 microM) and initiated action potential firing. The K+ channel opener diazoxide, but not cromakalim or pinacidil, inhibited electrical activity and increased the whole-cell K+ conductance fourfold. ATP applied to the intracellular face of the membrane inhibited KATP channel activity with a Ki of 17 microM, an effect that could be counteracted by Mg-ADP and Mg-GDP. GTP and UTP did not affect KATP channel activity. Phosphatidylinositol 4,5-bisphosphate activated KATP channels inhibited by ATP after a delay of 90 s. In situ hybridisation demonstrated the expression of the mRNA encoding KATP channel subunits Kir6.2 and SUR1 but not Kir6.1 and SUR2. We conclude that rat pancreatic A-cells express KATP channels with the nucleotide-, sulphonylurea- and K+ channel-opener sensitivities expected for a channel formed by Kir6.2 and SUR1 subunits.

Type

Journal article

Journal

Pflugers Arch

Publication Date

09/1999

Volume

438

Pages

428 - 436

Keywords

ATP-Binding Cassette Transporters, Adenosine Diphosphate, Adenosine Triphosphate, Animals, Electrophysiology, Guanosine Diphosphate, Guanosine Triphosphate, Hypoglycemic Agents, Islets of Langerhans, Male, Membrane Potentials, Phosphatidylinositol 4,5-Diphosphate, Potassium Channel Blockers, Potassium Channels, Potassium Channels, Inwardly Rectifying, Rats, Rats, Inbred Lew, Receptors, Drug, Sulfonylurea Compounds, Sulfonylurea Receptors, Tolbutamide, Uridine Triphosphate