Rise in intracellular calcium concentration elicited by isradipine in Gin-1 cells.

We performed experiments to examine whether isradipine (Isr), a calcium antagonist, would raise the intracellular calcium concentration ([Ca2+]i) in Gin-1 cells and, if so, to elucidate the mechanism of the [Ca2+]i rise. Gin-1 cells, which are human normal gingival fibroblasts were used as the material. The [Ca2+]i was measured with the Ca2+-sensitive fluorescent dye fura-2/AM. Changes in the fluorescence intensity of fura-2 in the cells were recorded with a video-imaging analysis system. Isr concentration-dependently raised the [Ca2+]i. A Ca2+-free saline significantly inhibited the Isr-induced [Ca2+]i rise. Whereas Isr in Ca2+-containing solution weakly raised the [Ca2+]i by pretreatment with thapsigargin, an inhibitor of Ca2+ release from Ca2+ stores, the Ca2+-free saline plus thapsigargin completely depressed the Isr-induced [Ca2+]i rise. The same response was observed in the case of pretreatment with cyclopiazonic acid (1 microM), another inhibitor of Ca2+ release from the Ca2+ stores. Isr raises the [Ca2+]i in Gin-1 cells and that the Isr-induced [Ca2+]i rise is ascribable to both the Ca2+ influx through the plasma membrane and Ca2+ release from the intracellular Ca2+ store.