Objective— To investigate whether adenosine diphosphate (ADP)–derived adenosine might inhibit platelet aggregation, especially in the presence of a P2Y12 antagonist, where the effects of ADP at the P2Y12 receptor would be prevented.

Methods and Results— Platelet aggregation was measured in response to thrombin receptor activator peptide by platelet counting in platelet-rich plasma (PRP) and whole blood in the presence of ADP and the P2Y12 antagonists cangrelor, prasugrel active metabolite, and ticagrelor. In the presence of a P2Y12 antagonist, preincubation of PRP with ADP inhibited aggregation; this effect was abolished by adenosine deaminase. No inhibition of aggregation occurred in whole blood except when dipyridamole was added to inhibit adenosine uptake into erythrocytes. The effects of ADP in PRP and whole blood were replicated using adenosine and were directly related to changes in cAMP (assessed by vasodilator-stimulated phosphoprotein phosphorylation). All results were the same irrespective of the P2Y12 antagonist used.

Conclusion— ADP inhibits platelet aggregation in the presence of a P2Y12 antagonist through conversion to adenosine. Inhibition occurs in PRP but not in whole blood except when adenosine uptake is inhibited. None of the P2Y12 antagonists studied replicated the effects of dipyridamole in the experiments that were performed.

Adenosine derived from ADP can contribute to inhibition of platelet aggregation in the presence of a P2Y12 antagonist.

Antiplatelet agents are drugs that reduce the ability of platelets to engage in thrombus formation. They do so by reducing the ability of platelets to aggregate together and also by inhibiting other aspects of platelet function that collectively contribute to thrombus formation. Ideally, antiplatelet agents add to the natural means through which platelet function is regulated. There are some antiplatelet agents, especially aspirin and clopidogrel, which are already widely used as antithrombotic agents. Also there are newer agents, prasugrel and ticagrelor, that have been recently licensed and are now being used in place of clopidogrel in some patients. In addition there are some novel agents that are either already in development or are suitable candidates for development. This chapter describes the pharmacology of those antiplatelet agents that a physician is likely to encounter in clinical practice both now and in the foreseeable future.

Antiplatelet Agents: Current and Novel

PO-27 Raised levels of CD39 in leucocytosis result in marked inhibition of ADP-induced platelet aggregation via rapid ADP hydrolysis

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PO-27 Raised levels of CD39 in leucocytosis result in marked inhibition of ADP-induced platelet aggregation via rapid ADP hydrolysis