ROLE OF EXTRACELLULAR CALCIUM IN NEUTROPHIL DE-GRANULATION RESPONSES TO 1-O-ALKYL-2-O-ACETYL-SN-GLYCERO-3-PHOSPHOCHOLINE

Abstract

The rabbit polymorphonuclear neutrophil degranulation response to 1-O-alkyl-2-O-acetyl-sn-glycero-3-phosphocholine depends on extracellular Ca. In the absence of this bivalent cation, neutrophil suspensions pretreated with cytochalasin B responded to the lipid by releasing minimal amounts of lysozyme and .beta.-glucuronidase. Incremental increases in extracellular calcium over a range of 20-200 .mu.M led to increasing amounts of lipid-stimulated enzyme release. Extracellular Mg neither supported nor enhanced the degranulation responses. Verapamil (25-200 .mu.g/ml), a Ca channel blocker, inhibited degranulation. Neutrophil suspensins exposed to the phosphocholine stimulus rapidly took up radiolabeled extracellular Ca. The kinetics of this Ca uptake were similar to the kinetics of enzyme release, and the amount of Ca taken up correlated closely with the amount of released lysozyme and .beta.-glucuronidase. Finally, in a dosage which blocked degranulation, verapamil inhibited Ca uptake. The rapid association of extracellular Ca with the neutrophil may mediate, at least in part, the degranulating actions of the phosphocholine stimulus.