Role of extracellular calcium and neutrophil degranulation responses to 1-O-alkyl-2-O-acetyl-sn-glycero-3-phosphocholine.

The rabbit polymorphonuclear neutrophil degranulation response to 1-O-alkyl-2-O-acetyl-sn-glycero-3-phosphocholine depends on extracellular calcium. 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 microM led to increasing amounts of lipid-stimulated enzyme release. In contrast, extracellular magnesium neither supported nor enhanced the degranulation responses. Verapamil (25-200 microgram/ml), a calcium channel blocker, inhibited degranulation. Neutrophil suspensions exposed to the phosphocholine stimulus rapidly took up radiolabeled extracellular calcium. The kinetics of this calcium uptake were similar to the kinetics of enzyme release, and the amount of calcium taken up correlated closely with the amount of released lysozyme and beta-glucuronidase. Finally, in a dosage which blocked degranulation, verapamil inhibited calcium uptake. Thus, the rapid association of extracellular calcium with the neutrophil may mediate, at least in part, the degranulating actions of the phosphocholine stimulus.