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• W1798325051 abstract "Summary ADP is considered a weak platelet agonist due to the limited aggregation responses it induces in vitro at physiological concentrations of extracellular Ca 2+ [(Ca 2+ ) o ]. Lowering [Ca 2+ ] o paradoxically enhances ADP‐evoked aggregation, an effect that has been attributed to enhanced thromboxane A 2 production. This study examined the role of ectonucleotidases in the [Ca 2+ ] o ‐dependence of platelet activation. Reducing [Ca 2+ ] o from millimolar to micromolar levels converted ADP (10 μmol/l)‐evoked platelet aggregation from a transient to a sustained response in both platelet‐rich plasma and washed suspensions. Blocking thromboxane A 2 production with aspirin had no effect on this [Ca 2+ ] o ‐dependence. Prevention of ADP degradation abolished the differences between low and physiological [Ca 2+ ] o resulting in a robust and sustained aggregation in both conditions. Measurements of extracellular ADP revealed reduced degradation in both plasma and apyrase‐containing saline at micromolar compared to millimolar [Ca 2+ ] o . As reported previously, thromboxane A 2 generation was enhanced at low [Ca 2+ ] o , however this was independent of ectonucleotidase activity . P2Y receptor antagonists cangrelor and MRS2179 demonstrated the necessity of P2Y 12 receptors for sustained ADP‐evoked aggregation, with a minor role for P2Y 1 . In conclusion, Ca 2+ ‐dependent ectonucleotidase activity is a major factor determining the extent of platelet aggregation to ADP and must be controlled for in studies of P2Y receptor activation." @default.
• W1798325051 created "2016-06-24" @default.
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• W1798325051 creator A5011869846 @default.
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• W1798325051 date "2011-02-20" @default.
• W1798325051 modified "2023-10-18" @default.
• W1798325051 title "Extracellular Ca2+ modulates ADP-evoked aggregation through altered agonist degradation: implications for conditions used to study P2Y receptor activation" @default.
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• W1798325051 doi "https://doi.org/10.1111/j.1365-2141.2010.08499.x" @default.
• W1798325051 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3084511" @default.
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