Abstract
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.