Effects of a calcium channel agonist on the electrical, ionic and secretory events in mouse pancreatic B-cells.
The changes in pancreatic B-cell function produced by a Ca channel agonist, the dihydropyridine derivative CGP 28392, have been studied with mouse islets. CGP 28392 (5 microM) modified the electrical activity induced in B-cells by 10 mM glucose: the duration and the amplitude of the slow waves of membrane potential increased, but the overall spike activity decreased. Simultaneously, CGP 28392 markedly increased insulin release and 45Ca2+ efflux, and slightly accelerated 86Rb+ efflux from islet cells. These latter effects were abolished by omission of extracellular Ca2+. Qualitatively similar changes were observed at 15 mM glucose, whereas CGP 28392 was ineffective at 3 mM glucose. These results strongly suggest that an influx of Ca2+ contributes to the slow waves of membrane potential triggered by glucose, and underline the importance of this influx of Ca2+ for the control of insulin release by the sugar.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002118:Calcium / Q000378:metabolism / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D005260:Female; D005947:Glucose / Q000494:pharmacology; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects / Q000502:physiology*; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D011725:Pyridines / Q000494:pharmacology*; D011868:Radioisotopes; D012413:Rubidium / Q000378:metabolism
D002121:Calcium Channel Blockers; D007328:Insulin; D011725:Pyridines; D011868:Radioisotopes; C040525:CGP 28392; D005947:Glucose; D012413:Rubidium; D002118:Calcium