@entity2819 enhances adrenocorticotropin-induced calcium signals in XXXX adrenocortical cells.

@entity230 @entity4235 @entity1880 @entity6239 @entity2819 @entity134 @entity141 @entity291 @entity855
The rapid effects of @entity134 hormones on @entity141 signals have been examined in @entity291 adrenocortical cells. Among the @entity134 molecules tested, only @entity2819 rapidly stimulated @entity141 signals upon addition of ACTH, although @entity2819 alone did not induce @entity141 signals. @entity2819 also enhanced steroidogenesis induced by ACTH. The enhancement of ACTH-induced @entity141 signals was also observed with membrane-impermeable @entity2819 conjugated to BSA and was not inhibited by @entity1880 . In addition, @entity2819 did not enhance @entity141 signals induced by @entity855 or angiotensin II. These results suggest that @entity2819 selectively stimulates ACTH-induced @entity141 signals in a nongenomic way by acting on a target in the plasma membrane. Furthermore, the supernatants of cells incubated with ACTH or @entity855 enhanced @entity141 signals, suggesting that @entity230 produced by such treatment act in an autocrine fashion. Consistent with this idea, these effects were inhibited by inhibitors of steroidogenesis ( @entity6239 or @entity4235 ). These results show that @entity134 molecules synthesized in adrenocortical cells facilitate ACTH-induced @entity141 signals. Taken together, @entity2819 secreted from adrenocortical cells activates ACTH-induced @entity141 signals and steroidogenesis by nongenomic means.
