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Study of aggregation of platelets lacking the P2Y1 receptor

The recent generation of mice deficient for the P2Y1 receptor has allowed us to directly examine the contribution of this nucleotide receptor in ADP‐induced aggregation both in isolated platelets and in vivo thrombosis. Studies utilizing the P2Y1‐deficient platelets clearly demonstrated that the P2Y1 receptor alone is not sufficient for describing the various effects induced by ADP on platelets. While no increase in intracellular calcium was observed in the platelets lacking P2Y1, the ability of ADP to decrease intracellular cAMP was unaltered. An additive and unexpected observation is the partial aggregation induced by exposure of P2Y1‐deficient platelets to high levels of ADP. This suggests that additional ADP receptors are expressed by platelets and that these receptors can induce partial aggregation of platelets in the absence of measurable changes in intracellular calcium. This review summarizes the recent advances in understanding the mechanisms involved in the platelet response to ADP and examines various hypotheses that attempt to explain the pathway leading to partial aggregation of P2Y1 platelets in response to ADP. Drug Dev. Res. 52:150–155, 2001. © 2001 Wiley‐Liss, Inc.