The changes in pancreatic B-cell function produced by a Ca channel agonist, the dihydropyridine derivative CGP 28392, have been studied with mouse islets. CGP 28392 (5 microM) modified the electrical activity induced in B-cells by 10 mM glucose: the duration and the amplitude of the slow waves of membrane potential increased, but the overall spike activity decreased. Simultaneously, CGP 28392 markedly increased insulin release and 45Ca2+ efflux, and slightly accelerated 86Rb+ efflux from islet cells. These latter effects were abolished by omission of extracellular Ca2+. Qualitatively similar changes were observed at 15 mM glucose, whereas CGP 28392 was ineffective at 3 mM glucose. These results strongly suggest that an influx of Ca2+ contributes to the slow waves of membrane potential triggered by glucose, and underline the importance of this influx of Ca2+ for the control of insulin release by the sugar.