The ionic, electrical, and secretory effects of protein kinase C activation in XXXX pancreatic B-cells: studies with a @entity4621 .

@entity268 @entity19 @entity4621 @entity865 @entity141 @entity864 @entity413
The @entity4621 @entity864 ( @entity865 ) was used to study the effects of protein kinase C activation on stimulus-secretion coupling in @entity19 pancreatic B-cells. At a nonstimulatory concentration of @entity413 (3 mM), 100 nM @entity865 , but not 10 nM @entity865 , slightly and slowly increased insulin release and 45Ca2+ efflux and decreased 86Rb+ efflux, but did not affect the membrane potential of B-cells. At a threshold concentration of @entity413 (7 mM), 100 nM @entity865 markedly increased insulin release without triggering electrical activity in B-cells. At a stimulatory concentration of @entity413 (10 mM), @entity865 caused a dose-dependent irreversible increase in insulin release, 45Ca2+ efflux, and 86Rb+ efflux and slightly augmented islet @entity268 levels. Omission of extracellular @entity141 abolished the effects of 10 nM @entity865 and partially inhibited those of 100 nM @entity865 on insulin release and 45Ca2+ efflux. In contrast, their effect on 86Rb+ efflux was paradoxically augmented. @entity413 -induced electrical activity in B-cells was only marginally affected by @entity865 ; the duration of the slow waves with spikes was not modified, but a small shortening of the polarized intervals raised their frequency and slightly increased the overall activity. This increase was significant only with 10 nM @entity865 , whereas only 100 nM @entity865 brought about a minute increase in 45Ca2+ influx. These results thus show that @entity865 induces insulin release or potentiates @entity413 -induced insulin release without mimicking or amplifying the initial ionic and electrical signals triggered by @entity413 . They suggest that protein kinase C activation affects stimulus-secretion coupling by modulating intracellular and/or nonelectrogenic membrane events.
