P2T Purinoceptors: ADP Receptors on Platelets

  1. Derek J. Chadwick Organizer and
  2. Jamie A. Goode
  1. Susanna M. O. Hourani and
  2. David A. Hall

Published Online: 28 SEP 2007

DOI: 10.1002/9780470514900.ch3

Ciba Foundation Symposium 198 - P2 Purinoceptors: Localization, Function and Transduction Mechanisms

Ciba Foundation Symposium 198 - P2 Purinoceptors: Localization, Function and Transduction Mechanisms

How to Cite

Hourani, S. M. O. and Hall, D. A. (2007) P2T Purinoceptors: ADP Receptors on Platelets, in Ciba Foundation Symposium 198 - P2 Purinoceptors: Localization, Function and Transduction Mechanisms (eds D. J. Chadwick and J. A. Goode), John Wiley & Sons, Ltd., Chichester, UK. doi: 10.1002/9780470514900.ch3

Author Information

  1. Receptors and Cellular Regulation Research Group, School of Biological Sciences, University of Surrey, Guildford, Surrey GU2 5XH, UK

  1. The Biological Laboratory, The University, Canterbury, Kent CT2 7NJ, UK

Publication History

  1. Published Online: 28 SEP 2007

ISBN Information

Print ISBN: 9780471961253

Online ISBN: 9780470514900

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Keywords:

  • P2T purinoceptors;
  • Ca2+ influx;
  • platelet ADP receptor;
  • platelet activation;
  • structure-activity relationships

Summary

ADP acts on platelets via the P2T purinoceptor to cause aggregation, but the way in which it does so is not fully understood. Most aggregating agents act via G protein-coupled receptors to stimulate phospholipase C (PLC) and so mobilize Ca2+ via inositol trisphosphate, whereas ADP clearly causes the mobilization of Ca2+ from internal stores but is only a weak activator of PLC. ADP also inhibits adenylate cyclase and it has been suggested that this effect is mediated by a different receptor, although evidence from antagonist studies argues against this. Studics of Ca2+ influx have shown that ADP is unique in causing a rapid influx of Ca2+, and patch-clamp studies have confirmed the activation by ADP of non-selective cation channels. This would imply the existence of two ADP receptors on platelets, a receptor-operated channel responsible for the rapid Ca2+ influx and a G protein-coupled receptor possibly linked to both inhibition of adenylate cyclase and mobilization of Ca2+. In this review the structure-activity relationships for aggregation, inhibition of adenylatc cyclase and increases in cytoplasmic Ca2+ are summarized, and the relationship between these effects discussed.