par Lebrun, Philippe 
;Malaisse, Willy ;Herchuelz, André
Référence The American journal of physiology, 242, 1, page (E59-E66)
Publication Publié, 1982-01
;Malaisse, Willy ;Herchuelz, André Référence The American journal of physiology, 242, 1, page (E59-E66)
Publication Publié, 1982-01
Article révisé par les pairs
| Résumé : | The pathways through which glucose stimulates Ca2+ inflow into islet cells were investigated by comparing the inhibitory effect of verapamil, a selective blocker of voltage-sensitive Ca2+ channels, on glucose- and K+-stimulated insulin release and 45Ca efflux from perifused rat pancreatic islets. The islets stimulated by K+ (20 mM) were more sensitive to verapamil than those exposed to glucose (27.8 mM). The stimulation of 45Ca efflux by a low concentration of glucose (8.3 mM) was extremely resistant to verapamil, whereas that induced by a rise in the glucose concentration from 8.3 to 27.8 mM displayed the same sensitivity towards verapamil as that characterizing the response to K+. Because the increase in 45Ca efflux evoked by glucose or K+. Because the increase in 45Ca efflux evoked by glucose or K+ reflects a stimulation of Ca2+ entry into islet cells, it is proposed that the B cell may be equipped with two populations of Ca2+ channels that differ in their sensitivity towards verapamil and possibly their voltage-dependency. Glucose apparently stimulates Ca2+ inflow through both types of channels. At low concentrations, glucose may stimulate Ca2+ inflow, in part, by gating the voltage-insensitive pathway. |
