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Regulation of calcium fluxes in pancreatic islets: glucose-induced calcium-calcium exchange.

Glucose provokes an initial fall followed by a secondary rise in 45Ca efflux from prelabeled pancreatic islets. Prior exposure of the islets to calcium-depleted media does not suppress the secondary rise, provided that the extracellular calcium concentration is normalized 2 min before addition of glucose. Such a treatment significantly reduces insulin release. The secondary rise, as distinct from the initial fall, is inhibited under conditions known to interfere with calcium entry into the beta-cell, e.g., in the presence of ruthenium red or cobalt. Calcium itself in high concentrations provokes a dramatic increase in 45Ca efflux. The magnitude of this calcium-induced efflux is enhanced by prior exposure of the islets to calcium-depleted media. Imidazole and the theophylline do not modify the effect of glucose on 45Ca efflux. It is proposed that the glucose-induced secondary rise in 45Ca efflux corresponds to a calcium-calcium exchange process in which influent 40Ca displaces 45Ca from intracellular sites.