Abstract:
:Adenosine diphosphate (ADP) is recognized as an important mediator of platelet aggregation. Transient aggregation at low (< or =1 microM), and sustained aggregation at higher ADP concentrations are consistently observed. Dissociation of platelet aggregates has been described and may explain the reversible component of the aggregation response. We hypothesized that the net aggregation response to ADP in vitro results from the concurrent activation of two opposing processes, aggregation and deaggregation. Different purinergic receptor subtypes may mediate these effects. To test this hypothesis and its generalizability, we performed a kinetic analysis of representative published ADP-induced aggregation responses supplemented with original data from our laboratory. A four-compartment kinetic model was used to estimate k(3), a rate constant of deaggregation. Two model-independent parameters, the magnitude of the aggregation response (DeltaOD) and the time to reach maximal aggregation (t(peak)) were also assessed. Greater sustained aggregation at higher ADP concentrations was consistently associated with increased DeltaOD and t(peak) but decreased k(3) values. These relationships were independent of type of platelet preparation or experimental conditions and not due to ADP receptor desensitization. Conversely, blockade of the P2Y(12) receptor subtype (ticlopidine, clopidogrel or 2-MeS-AMP) decreased DeltaOD and t(peak) but increased k(3) values. This supports the presence of active deaggregation which is decelerated by activation of the P2Y(12) receptor subtype.
journal_name
Plateletsjournal_title
Plateletsauthors
Maayani S,Tagliente TM,Schwarz T,Craddock-Royal B,Alcala C,Marrero G,Martinez Rdoi
10.1080/09537100120071004subject
Has Abstractpub_date
2001-08-01 00:00:00pages
279-91issue
5eissn
0953-7104issn
1369-1635journal_volume
12pub_type
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