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Platelet-activating factor (PAF)-induced platelet aggregation. Modulation by plasma adenosine and methylxanthines
K C Agarwal1, E Clarke, S Rounds
1Section of Molecular and Biochemical Pharmacology, Brown University, Providence, RI 02912.
Biochemical Pharmacology
|November 16, 1994
Summary
Plasma adenosine significantly modulates platelet-activating factor (PAF) activity. Lowering adenosine boosts PAF
Area of Science:
- Biochemistry
- Pharmacology
- Hematology
Background:
- Platelet-activating factor (PAF) is a potent mediator of platelet aggregation and serotonin release.
- The role of plasma adenosine in modulating PAF activity requires further elucidation.
Purpose of the Study:
- To investigate the inhibitory role of plasma adenosine on PAF-induced platelet aggregation and serotonin release.
- To examine the effects of methylxanthines, adenosine antagonists, on PAF activity in human platelets.
Main Methods:
- Human platelet-rich plasma (PRP) was used to study platelet aggregation and serotonin release.
- Adenosine levels were manipulated (depleted or normal) to assess PAF activity.
- Theophylline, caffeine, and DMPX were used as adenosine antagonists.
Main Results:
- Plasma adenosine (0.1–0.3 microM) significantly inhibits PAF-induced platelet aggregation and serotonin release.
- Adenosine depletion increased PAF's platelet-aggregating activity over 10-fold.
- Adenosine antagonists (theophylline, caffeine, DMPX) potentiated PAF activity; patients on theophylline showed enhanced aggregation.
Conclusions:
- Plasma adenosine plays a crucial role in negatively modulating PAF activity on platelets.
- Adenosine is a more potent inhibitor of serotonin release than platelet aggregation.
- Agents modulating plasma adenosine or methylxanthines could be therapeutically relevant for controlling PAF actions.