Ca2+ entry induced by calcium influx factor and its regulation by protein kinase C in rabbit neutrophils

Extracellular application of acid extract from platelet-activating factor or thapsigargin-treated rabbit neutrophils induced a rise of cytosolic free calcium concentration ([Ca2+](i)) in neutrophils and adrenal chromaffin cells suspended in Ca2+ containing, but not in Ca2+ deficient, medium. The ability of the extract to selectively induce Ca2+ entry was also confirmed by the increase in Ca-45(2+) uptake and failure to stimulate Ca2+ release in digitonin permeabilized neutrophils. 12-O-tetradecanoylphorbol-13-acetate (TPA) inhibited the extract-induced [Ca2+](i) rise in a staurosporine (ST)-sensitive fashion, neither of which had any effect on its production. SK&F 96365 and econazole also reduced extract-induced Ca2+ entry. These results suggest that a Ca2+ entry-inducible substrate (calcium influx factor) is extracted from Ca2+ store-depleted neutrophils, and that its action may be regulated by protein kinase C and certain pharmacological agents.