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.
D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D002118:Calcium / Q000378:metabolism* / Q000494:pharmacology; D003035:Cobalt / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D005947:Glucose / Q000494:pharmacology*; D066298:In Vitro Techniques; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000378:metabolism*; D051381:Rats; D012430:Ruthenium Red / Q000494:pharmacology; D014700:Verapamil / Q000494:pharmacology
D007328:Insulin; D012430:Ruthenium Red; D003035:Cobalt; D014700:Verapamil; D005947:Glucose; D002118:Calcium