Fig. 3.
Fig. 3. Effect of receptor-specific antagonists on GPVI-mediated platelet aggregation. / Washed, aspirin-treated human platelets were treated with various antagonists (as indicated), then challenged with various concentrations of convulxin (A), CRP (B), and collagen (C). Extent of aggregations were measured 210 seconds after the addition of the agonist, in the absence of any antagonist (●), in the presence of a P2Y1 antagonist (○), a P2Y12 antagonist (■), or both P2Y1 and P2Y12 antagonists (▪). The maximum aggregation extent in the absence of any antagonist was taken as 100% and the remaining values were normalized to this value. In the case of collagen, extent of aggregation in the presence of SC57101, a fibrinogen receptor antagonist, was taken as zero. Concentrations of agents used were: P2Y1 antagonists A3P5P, 1 mM (A) or MRS2179, 100 μM (B,C); P2Y12 antagonists AR-C66096, 1 μM (A) or AR-C69931MX, 100 nM (B,C). Each data point is the mean ± SE of 3 measurements with different donors.

Effect of receptor-specific antagonists on GPVI-mediated platelet aggregation.

Washed, aspirin-treated human platelets were treated with various antagonists (as indicated), then challenged with various concentrations of convulxin (A), CRP (B), and collagen (C). Extent of aggregations were measured 210 seconds after the addition of the agonist, in the absence of any antagonist (●), in the presence of a P2Y1 antagonist (○), a P2Y12 antagonist (■), or both P2Y1 and P2Y12 antagonists (▪). The maximum aggregation extent in the absence of any antagonist was taken as 100% and the remaining values were normalized to this value. In the case of collagen, extent of aggregation in the presence of SC57101, a fibrinogen receptor antagonist, was taken as zero. Concentrations of agents used were: P2Y1 antagonists A3P5P, 1 mM (A) or MRS2179, 100 μM (B,C); P2Y12 antagonists AR-C66096, 1 μM (A) or AR-C69931MX, 100 nM (B,C). Each data point is the mean ± SE of 3 measurements with different donors.

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