Article révisé par les pairs
Résumé : The absence of extracellular K + modifies glucose-induced insulin secretion. The dynamics of these changes was studied in isolated rat islets perifused with K +-deprived media containing various Na + concentrations. Omission of K + from the perifusate during stimulation with 300 mg glucose/100 ml did not cause significant changes in IRI secretion, when Na + concentration was normal (149 mM Na +). If external Na + was partially substituted (24 mM Na +) by choline, a decrease in the amplitude of the second phase of release was noted. Both phases were markedly depressed, when Na + was reduced to 2 mM. Removal of K + for 25 min before glucose stimulation resulted in an acceleration and potentiation of the early phase of release, contrasting with the progressive inhibition of the late one. This inhibition was slowly reversible 10 min after K + reintroduction. Under the same experimental conditions, decrease of Na + concentration to 24 mM slowed and inhibited the first phase of secretion, and depressed further the second phase, without alteration of the dynamics of secretion. Glucose oxidation by islets was reduced by 35% after 2 h of incubation in a K +-free medium; this inhibition was more pronounced (65%) after 1 h, when the islets were previously perifused for 60 min in the absence of K +. From these results, it is suggested that changes in glucose-induced secretion observed in the absence of K +, are secondary to the intracellular modifications of Na + and K + concentrations due to the decreased activity of the Na +/K +) pump. They seem to be the result of two antagonistic effects: a facilitation of secretion by Na + accumulation and an inhibition by K + depletion. © 1974 Springer-Verlag.