Another secondary agonist for platelets is adenosine diphosphate (ADP) which is released from platelet dense granules in response to the primary agonists (McNicol and Israels, 1999) (Figure 1). Adenine nucleotides and nucleosides [adenosine triphosphate (ATP), ADP and adenosine] modulate platelet aggregation, shape change and the release of alpha granules (Enjyoji et al., 1999; Burnstock, 2017). The role of ATP, ADP, and adenosine in platelet function is controlled by an organized enzymatic chain, including ecto-nucleoside triphosphate diphosphohydrolase (CD39) and ecto-5′-nucleotidase (CD73), which catalyzes the hydrolysis of released ATP into ADP, adenosine monophosphate (AMP) and finally to adenosine (Bakker et al., 1994; Robson et al., 2006; Burnstock, 2017). Extracellular nucleotides act on platelets through distinct receptors belonging to the P2 ATP family: the P2Y1 and P2Y12 metabotropic, G protein-coupled receptors, involved in transient platelet shape change and platelet aggregation (Burnstock, 1972) and the P2X1 ionotropic receptor (Burnstock, 1972; Cattaneo et al., 2002; Oury et al., 2004; Gachet, 2012) (Figure 1).