Abstract
1-Alkyl-2-acetyl- sn-glycero-3-phosphocholine (platelet-activating factor) induces an increase of Ca 2+ uptake in rabbit platelets. This process depends upon the extracellular concentration of Ca 2+ with the maximum stimulation occurring at 1–3 m m; uptake under these conditions is blocked by verapamil, a calcium-entry blocker. Increase of calcium uptake by the bioactive phospholipid was independent of ADP-induced platelet responses and of metabolites of arachidonic acid metabolism formed through the cyclooxygenase pathway. However, mepacrine, p-bromophenacyl bromide, eicosatetraynoic acid, and nordihydroguaiaretic acid significantly or totally inhibited the stimulation of Ca 2+ uptake by 1-alkyl-2-acetyl- sn-glycero-3-phosphocholine. When arachidonic acid was given sufficient time to be metabolized to other products by the platelets, stimulation of Ca 2+ uptake also occurred. Arachidonic acid and platelet-activating factor did not produce an additive or synergistic effect. Our data suggest that a metabolite(s) generated from arachidonic acid through the lipoxygenase pathway may be the mediator(s) responsible for the action of platelet-activating factor in the induction of increased Ca 2+ uptake in rabbit platelets.
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