Contribution of ADP to the amplification of primary platelet aggregation by platelet activating factor (PAF): modulatory role of aspirin.
Platelet Activating Factor (PAF)-induced human platelet aggregation in citrated plasma is accompanied by activation of the cyclo-oxygenase pathway and release of intracellular constituents including Adenosine-5'-diphosphate (ADP). Inhibition of the cyclo-oxygenase pathway by aspirin prevented the amplification of primary platelet aggregation induced by threshold concentrations of PAF. Removal of ADP by enzymatic systems had little or no effect on PAF-induced full aggregation, but reversed the aggregating effect of PAF (at 10 times threshold concentrations) on 'aspirinated' platelets. Aspirin also prevented the synergism between PAF and ADP when subthreshold concentrations of both compounds were combined. Similar results were obtained in heparinized platelet-rich plasma. Thus, ADP may amplify the primary response to PAF but its role is modulated by the availability of the cyclo-oxygenase pathway products.
D
D
Lauri
C
C
Cerletti
G
G
de Gaetano
D000244:Adenosine Diphosphate / Q000494:pharmacology*; D001241:Aspirin / Q000494:pharmacology*; D003402:Creatine Kinase / Q000494:pharmacology; D004347:Drug Interactions; D006801:Humans; D007700:Kinetics; D010725:Phosphocreatine / Q000494:pharmacology; D010972:Platelet Activating Factor / Q000494:pharmacology*; D010974:Platelet Aggregation / Q000187:drug effects*
D010972:Platelet Activating Factor; D010725:Phosphocreatine; D000244:Adenosine Diphosphate; D003402:Creatine Kinase; D001241:Aspirin