September 1, 2000British Journal of Haematology
The central role of the P2T receptor in amplification of human platelet activation, aggregation, secretion and procoagulant activity
Key result
P2T receptor activation amplified ADP-induced aggregation initiated by the P2Y1 receptor, as well as amplifying aggregation, secretion and procoagulant responses induced by other agonists.
Why the study?
Does P2T receptor antagonism with AR-C69931MX inhibit human platelet activation, aggregation, secretion, and procoagulant activity?
Population
Human platelets
Comparison
AR-C69931MX (selective P2T receptor antagonist) vs A2P5P (selective P2Y1 antagonist) and aspirin
Design
Preclinical
Authors
Discussion
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Member takes
Implication
Animal data position P2T receptor as platelet response amplifier; leaves open translation to human P2Y12 antagonist efficacy.
Structured PICO
Does P2T receptor antagonism with AR-C69931MX inhibit human platelet activation, aggregation, secretion, and procoagulant activity?
P
Population
Human platelets
I
Intervention
AR-C69931MX (selective P2T receptor antagonist)
C
Comparator
A2P5P (selective P2Y1 antagonist) and aspirin
O
Outcome
Platelet aggregation, dense granule release, Ca2+ mobilization, P-selectin expression, Annexin V binding, and microparticle formationsurrogate
The P2T receptor plays a central role in amplifying platelet responses, highlighting the mechanistic basis and clinical potential of P2T (P2Y12) receptor antagonists as antithrombotic agents.
Cite This Study
Storey et al. (2000) studied this question. AR-C69931MX (P2T receptor antagonist) was evaluated on Platelet activation, aggregation, secretion and procoagulant activity. P2T receptor activation amplified ADP-induced aggregation initiated by the P2Y1 receptor, as well as amplifying aggregation, secretion and procoagulant responses induced by other agonists.