PLATELET-ACTIVATING-FACTOR MEDIATED POTENTIATION OF STIMULATION-EVOKED CATECHOLAMINE RELEASE AND THE RISE IN INTRACELLULAR FREE CA2+ CONCENTRATION IN ADRENAL CHROMAFFIN CELLS

The effects of platelet-activating factor (PAF) on catecholamine (CA) release and intracellular free Ca2+ concentration ([Ca2+](i)) were studied in cultured bovine adrenal chromaffin cells. PAF (1 nM-1 mu M) alone had no effect on [Ca2+](i) and basal CA release, but potentiated the [Ca2+](i) rise and CA release evoked by acetylcholine (ACh) and by elevated extracellular K+. PAF did not potentiate the responses to caffeine in Ca2+-deficient medium or to Bay K 8644. In chromaffin cells pretreated with either BN 50739, tetrodotoxin and amiloride or in Na+-deficient medium, PAF failed to potentiate the stimulation-evoked [Ca2+](i) rise and CA release. In contrast, neomycin, U 73122, 5-(N-ethyl-N-isopropyl)amiloride or pertussis toxin were ineffective in blocking the potentiating effect of PAF. In a membrane fraction prepared from fresh bovine adrenal medulla, ligand-binding studies using [H-3]WEB 2086 identified a PAF-displaceable binding site. These results are consistent with a model in which PAF modulates CA release by activating plasmamembrane receptors that can enhance the [Ca2+](i) rise via an Na+-dependent mechanism.