Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Purinoceptors and platelet aggregation

S M Hourani1

  • 1School of Biological Sciences, University of Surrey, Guildford, UK.

Journal of Autonomic Pharmacology
|December 1, 1996
PubMed
Summary

Adenosine 5'-diphosphate (ADP) mediates platelet aggregation through purinoceptors, but its exact mechanisms and the role of adenosine 5'-triphosphate (ATP) remain unclear. Research suggests multiple ADP receptors, including G protein-coupled and cation channels, influencing platelet activation and calcium signaling.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Role of cyclic nucleotides in vasodilations of the rat thoracic aorta induced by adenosine analogues.

British journal of pharmacology·2001
Same author

Characterisation of adenosine receptors mediating relaxation in hamster isolated aorta.

Naunyn-Schmiedeberg's archives of pharmacology·2000
Same author

Platelet P2 receptors: from curiosity to clinical targets.

Journal of the autonomic nervous system·2000
Same author

Breakdown of extracellular ATP by the prostatic and epididymal ends of the guinea pig vas deferens.

European journal of pharmacology·2000
Same author

Effects of allopurinol, erythro-9-(2-hydroxy-3-nonyl)adenine and S-(4-nitrobenzyl)-6-thioinosine on the degradation of adenosine 5'-triphosphate in the rat colon muscularis mucosae.

Journal of autonomic pharmacology·1999
Same author

Effects of noradrenaline, the calcium ionophore A23187, forskolin, sodium nitroprusside and glibenclamide on the degradation of extracellular adenosine 5'-triphosphate by the rat isolated vas deferens.

Journal of autonomic pharmacology·1999

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Pharmacology

Background:

  • Adenosine 5 '-diphosphate (ADP) is a key mediator released from damaged cells and aggregating platelets.
  • ADP signaling in platelets occurs via purinoceptors, with adenosine 5 '-triphosphate (ATP) acting as a competitive antagonist, though the precise mechanisms are not fully elucidated.
  • ADP elicits diverse cellular responses, including G12 protein activation, weak phospholipase C activation, calcium mobilization, and adenylate cyclase inhibition, potentially mediated by a single receptor type.

Purpose of the Study:

  • To investigate the complex mechanisms of ADP-induced platelet aggregation.
  • To clarify the roles of different purinoceptors in mediating ADP's effects on platelets.
  • To understand the interplay between ADP, ATP, and adenosine in regulating platelet function.

Related Experiment Videos

Main Methods:

  • Analysis of ADP's effects on platelet signaling pathways, including G protein activation, phospholipase C activity, and calcium mobilization.
  • Investigation of ADP-induced calcium influx and its potential association with P2X1 receptors.
  • Exploration of the role of adenosine receptors (A2a) and ectonucleotidases in modulating platelet activity.

Main Results:

  • ADP activates G12 proteins, weakly activates phospholipase C, mobilizes intracellular calcium, and inhibits adenylate cyclase.
  • ADP induces rapid calcium influx, characteristic of a receptor-operated channel, possibly mediated by a P2X1 receptor.
  • Platelet-derived ADP is metabolized to adenosine by endothelial ectonucleotidases, which stimulates A2a receptors to inhibit platelet activation.

Conclusions:

  • Platelet activation by ADP likely involves at least two receptor types: a G protein-coupled receptor and a cation channel (P2X1 receptor).
  • The breakdown of ADP to adenosine by endothelial cells represents a crucial mechanism for limiting platelet aggregation in intact blood vessels.
  • Further research is needed to fully elucidate the distinct roles of these receptors and the precise contribution of ATP in platelet function.