title: The role of plasma membrane K+ and Ca2+ permeabilities for glucose induction of slow Ca2+ oscillations in pancreatic beta-cells.
abstract: In individual pancreatic beta-cells the rise of the cytoplasmic Ca2+ concentration ([Ca2+]i), induced by 11 mM glucose, is manifested either as oscillations (0.2-0.5 min-1) or as a sustained elevation. The significance of the plasma membrane permeability of Ca2+ and K- for the establishment of these slow oscillations was investigated by dual wavelength microfluorometric measurements of [Ca2+]i in individual ob/ob mouse beta-cells loaded with fura-2. Increasing the extracellular Ca2+ to 10 mM or the addition of Ca2+ channel agonist BAY K 8644 (1 microM) or K+ channel blocker tetraethylammonium+ (TEA: 10-20 mM) caused steeper rises and higher peaks of the glucose-induced oscillations. However, when extracellular Ca2+ was lowered to 0.5 mM the oscillations were transformed into a sustained suprabasal level. When the beta-cells exhibited glucose-stimulated sustained elevation of [Ca2+]i in the presence of a physiological Ca2+ concentration (1.3 mM), it was possible to induce slow oscillations by promoting the entry of Ca2+ either by raising the extracellular Ca2+ concentration to 10 mM or adding TEA or BAY K 8644. The results indicate that glucose-induced slow oscillations of [Ca2+]i depend on the closure of ATP-regulated K+ channels and require that the rate of Ca2+ influx exceeds a critical level. Apart from an inherent periodicity in ATP production it is proposed that Ca(2+)-induced ATP consumption in the submembrane space contributes to the cyclic changes of the membrane potential determining periodic entry of Ca2+.
authors.affiliation: Department of Medical Cell Biology, Uppsala University, Sweden.
authors.forename: M
authors.initials: M
authors.lastname: Eberhardson
authors.forename: A
authors.initials: A
authors.lastname: Tengholm
authors.forename: E
authors.initials: E
authors.lastname: Grapengiesser
mesh_terms: D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000378:metabolism* / Q000494:pharmacology; D002120:Calcium Channel Agonists / Q000494:pharmacology; D002463:Cell Membrane Permeability / Q000502:physiology*; D005947:Glucose / Q000494:pharmacology*; D007515:Islets of Langerhans / Q000378:metabolism* / Q000648:ultrastructure; D051379:Mice; D008820:Mice, Obese; D010507:Periodicity; D011188:Potassium / Q000378:metabolism*; D015221:Potassium Channels / Q000187:drug effects; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology
chemical_list: D002120:Calcium Channel Agonists; D015221:Potassium Channels; D013757:Tetraethylammonium Compounds; D019789:Tetraethylammonium; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D005947:Glucose; D011188:Potassium; D002118:Calcium