par Lebrun, Philippe 
;Malaisse, Willy ;Herchuelz, André
Référence Diabetes (New York, N.Y.), 31, 11, page (1010-1015)
Publication Publié, 1982-11
;Malaisse, Willy ;Herchuelz, André Référence Diabetes (New York, N.Y.), 31, 11, page (1010-1015)
Publication Publié, 1982-11
Article révisé par les pairs
| Résumé : | The hypoglycemic sulfonylurea gliclazide stimulated 45Ca efflux and insulin release from prelabeled and perifused pancreatic rat islets, whether in the absence or presence of glucose (8.3 mM). The gliclazide-induced increase in 45Ca efflux is thought to reflect a stimulation of 40Ca influx into islet cells; it is suppressed in the absence of extracellular Ca2+ or in the presence of the organic CA2/-antagonist verapamil. In the absence of glucose, the ED50 for the inhibitory action of verapamil on gliclazide-stimulated 45Ca efflux was almost identical to that found when the process of 40Ca-45Ca exchange was stimulated by an increase in the extracellular concentration of K+, a procedure that leads to the depolarization of the plasma membrane. In the presence of glucose, however, the cationic response to gliclazide displayed an increased sensitivity toward the inhibitory action of verapamil. It is proposed that hypoglycemic sulfonylureas facilitate Ca2+ inflow into islet cells mainly through voltage-sensitive Ca2+ channels. In the presence of glucose, however, the stimulant action of hypoglycemic sulfonylureas upon Ca2+ entry into islet cells may entail a modality of Ca2+ transport not identical to that evoked by depolarization of the plasma membrane. |
