Evidence for two distinct modalities of CA2+ influx into pancreatic B cell.
The pathways through which glucose stimulates Ca2+ inflow into islet cells were investigated by comparing the inhibitory effect of verapamil, a selective blocker of voltage-sensitive Ca2+ channels, on glucose- and K+-stimulated insulin release and 45Ca efflux from perifused rat pancreatic islets. The islets stimulated by K+ (20 mM) were more sensitive to verapamil than those exposed to glucose (27.8 mM). The stimulation of 45Ca efflux by a low concentration of glucose (8.3 mM) was extremely resistant to verapamil, whereas that induced by a rise in the glucose concentration from 8.3 to 27.8 mM displayed the same sensitivity towards verapamil as that characterizing the response to K+. Because the increase in 45Ca efflux evoked by glucose or K+. Because the increase in 45Ca efflux evoked by glucose or K+ reflects a stimulation of Ca2+ entry into islet cells, it is proposed that the B cell may be equipped with two populations of Ca2+ channels that differ in their sensitivity towards verapamil and possibly their voltage-dependency. Glucose apparently stimulates Ca2+ inflow through both types of channels. At low concentrations, glucose may stimulate Ca2+ inflow, in part, by gating the voltage-insensitive pathway.
D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D002118:Calcium / Q000378:metabolism*; D005947:Glucose / Q000494:pharmacology; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D007473:Ion Channels / Q000378:metabolism; D007515:Islets of Langerhans / Q000187:drug effects / Q000378:metabolism*; D007700:Kinetics; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D014700:Verapamil / Q000494:pharmacology
D007328:Insulin; D007473:Ion Channels; D014700:Verapamil; D005947:Glucose; D011188:Potassium; D002118:Calcium