EFFECTS OF CALCIUM-CHANNEL BLOCKERS ON INSULIN-SECRETION AND CA-45(2+)-UPTAKE OF RAT ISLETS STIMULATED BY GLUCOSE OR K+-DEPOLARIZATION

Two calcium channel antagonists, verapamil and nifedipine, have been used to explore the dependence of secretion on voltage-gated influx of calcium. Both antagonists were able to suppress the secretory response to K+-depolarization as well as the stimulation of Ca-45(2+)-uptake. However, they inhibited only partially the stimulation of both secretion and Ca-45(2+)-uptake induced by glucose, alone or with palmitate. The stimulation of Ca-45(2+)-uptake by K+-depolarization, unlike that induced by glucose, was not sensitive to norepinephrine, starvation or fatty acid oxidation inhibitors. Therefore, it is suggested that glucose either modifies the properties of the voltage-dependent calcium channel and/or accelerates the exchange of a particular intracellular pool of calcium.