Regulation of calcium fluxes in rat pancreatic islets: dissimilar effects of glucose and of sodium ion accumulation

1. Removal of extracellular K+ provoked a dramatic increase in 43Ca efflux from pancreatic islets prelabelled in the presence of glucose. Such an increase in 45Ca efflux was preceded by a modest and transient reduction in 45Ca efflux. The increase in 45Ca efflux was reduced when the islets were perifused either in the presence of glucose 16 .7 mM or in the absence of extracellular Ca2+. It was abolished when the islets were perifused in the absence of extracellular Na+. 2. When the islets had been prelabelled in the absence as distinct from presence of glucose, the increase in 45Ca efflux observed on removal of extracellular K+ was of smaller amplitude. It was completely abolished when, in addition, Ca2+ was replaced by Co2+ in the perifusate. 3. Veratridine also provoked a dramatic increase in 45Ca efflux. This increase was slightly reduced when the perifusate contained glucose 5 .6 mM and markedly reduced in the absence of extracellular Ca2+. 4. Both the removal of extracellular K+ or addition of veratridine had little or no effect on insulin release in the absence of glucose. A significant increase in insulin release was observed, however, in the presence of glucose. The increase in insulin release, due to removal of extracellular K+, was completely abolished at low extracellular Na+ concentration. Such as ionic manipulation failed to affect veratridine-induced insulin release. Tetrodotoxin failed to inhibit glucose-stimulated insulin release. 5. It is concluded that Na+ accumulation in islet cells due to either veratridine or removal of extracellular K+ provokes the release of Ca2+ from intracellular stores but fails to reproduce the effect of glucose to reduce 45Ca efflux and to stimulate insulin release.In VitroJournal ArticleSCOPUS: NotDefined.jFLWIN