Abstract

The ability of the chemokines SDF-1, MDC and TARC to induce platelet aggregation depends strongly on low levels of ADP. The ADP receptors involved have now been characterized using the P2Y 1 and P2T AC receptor antagonists, A2P5P and AR-C69931MX. Stimulation of aggregation by the chemokines at 10 s was not blocked by AR-C69931MX, but was strongly inhibited by A2P5P. Pertussis toxin abolished the chemokine-stimulated aggregation. We conclude that the P2Y 1 ADP receptor plays a critical role in the initial phases of SDF-1-, MDC- and TARC-induced platelet aggregation, which involve a pertussis toxin-sensitive G protein.

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