Inhibitory effects of P2Y12 receptor antagonists on TRAP-induced platelet aggregation, procoagulant activity, microparticle formation and intracellular calcium responses in patients with acute coronary syndromes

Thrombin induces platelet aggregation and membrane rearrangements leading to enhanced procoagulant activity and microparticle production, all of which are thought to contribute to thrombus formation in patients with acute coronary syndromes (ACS). Clopidogrel, an adenosine diphosphate (ADP) receptor...

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Bibliographic Details
Published in:Platelets (Edinburgh) 2005-03, Vol.16 (2), p.73-80
Main Authors: Behan, Miles W. H., Fox, Susan C., Heptinstall, Stan, Storey, Robert F.
Format: Article
Language:English
Subjects:
Adenosine Monophosphate - analogs & derivatives
Adenosine Monophosphate - pharmacology
ADP-antagonists
calcium
Calcium Signaling - drug effects
Coronary Disease - drug therapy
Coronary Disease - metabolism
Dose-Response Relationship, Drug
Female
Humans
Male
Membrane Proteins - antagonists & inhibitors
Platelet Aggregation - drug effects
Platelet Aggregation Inhibitors - administration & dosage
platelets
procoagulant activity
Purinergic P2 Receptor Antagonists
Receptors, Purinergic P2Y12
Receptors, Thrombin - metabolism
thrombosis
Ticlopidine - administration & dosage
Ticlopidine - analogs & derivatives
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Summary:Thrombin induces platelet aggregation and membrane rearrangements leading to enhanced procoagulant activity and microparticle production, all of which are thought to contribute to thrombus formation in patients with acute coronary syndromes (ACS). Clopidogrel, an adenosine diphosphate (ADP) receptor antagonist acting at the P2Y12 receptor, has been shown to provide clinical benefit in ACS. We aimed to investigate the effects of clopidogrel ex vivo and another ADP-antagonist, AR-C69931MX in vitro on thrombin receptor activating peptide (TRAP)-induced platelet aggregation, procoagulant activity, microparticle formation and [Ca2+]i responses in patients with ACS. Measurements were performed in platelet-rich plasma using aggregometry and flow cytometry (n = 12). Clopidogrel (300 mg loading dose plus 75 mg daily) significantly inhibited TRAP-induced aggregation, procoagulant activity (annexin V binding) and microparticle production (all P 
ISSN:0953-7104
1369-1635
DOI:10.1080/09537100400005634