Semin Thromb Hemost 2005; 31(2): 139-149
DOI: 10.1055/s-2005-869519
Copyright © 2005 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel: +1(212) 584-4662.

Overview of the P2 Receptors

Jean-Marie Boeynaems1 , 2 , 3 , Didier Communi2 , Nathalie Suarez Gonzalez2 , Bernard Robaye2
  • 1Professor, Institute of Interdisciplinary Research, School of Medicine and Institute of Molecular and Medical Biology, Brussels, Belgium
  • 2Institute of Interdisciplinary Research, School of Medicine
  • 3Department of Medical Chemistry, Erasme Hospital, Université Libre de Bruxelles, Brussels, Belgium
Further Information

Publication History

Publication Date:
26 April 2005 (online)


The release of nucleotides in extracellular fluids can result from cell necrosis, exocytosis of secretory granules (such as platelet dense granules), or efflux through membrane channels. In addition, recent evidence suggests that vesicular trafficking is an important pathway of nucleotide release. Once in the extracellular fluids, they are rapidly degraded by ectonucleotidases, such as CD39, that play a key role in neutralizing the platelet aggregatory action of adenosine diphosphate (ADP), and act on two families of receptors: the ionotropic P2X receptors and the G-protein-coupled P2Y receptors. The family of P2X receptors encompasses seven genes. Currently, there are eight genuine P2Y receptors that can be subdivided into two structurally distinct subfamilies. Whereas P2X receptors are receptors of ATP, the different P2Y receptors are activated by distinct nucleotides, diphosphates or triphosphates, or purines or pyrimidines, some of them being conjugated to sugars. The study of knockout mice has demonstrated that P2X receptors play important roles in the neurogenic control of smooth muscle contraction, in pain and visceral perception, and in macrophage functions. The phenotype of P2Y null mice so far is more restricted: inhibition of platelet aggregation to ADP and increased bleeding time in P2Y1 -/- and P2Y12 -/- mice and lack of epithelial responsiveness to nucleotides in airways (P2Y2 -/-) and intestine (P2Y4 0/-).


Jean-Marie Boeynaems

Chimie Médicale, Hôpital Erasme

808, Route de Lennik, 1070 Brussels, Belgium