Key result
VK 744 inhibits human platelet aggregation induced by collagen and ADP in vitro.
Why the study?
The effect of VK 744, an analogue of dipyridamole, on human blood platelet function was not fully characterized.
Does VK 744 inhibit human blood platelet function in vitro?
Does VK 744 inhibit human blood platelet function in vitro?
VK 744 is a potent in vitro inhibitor of human platelet aggregation and function.
The effect of VK 744 (an analogue of dipyridamole) on the function of human blood platelets was studied. VK 744 inhibits collagen aggregation at a concentration of 25 μM. Preincubation at 37° C enhances the effect. ADP aggregation is inhibited at 50 μM. Adrenaline aggregation is likewise inhibited, and becomes reversible at 50 μM. VK 744 causes active disaggregation when added during ADP aggregation. The glass‐bead column retention and clot retraction are not inhibited until a concentration of 1 mM is attained. The glass adhesiveness according to Breddin is inhibited by 10 μM. The availability of platelet factor 3 as well as serotonin uptake are inhibited at the ED 50 of 6 μM and 0.2 mM, respectively. Comparison with RA 233 disclosed that two separate pharmacological receptors are involved. A study of serotonin release in collagen aggregation revealed that VK 744 is a primary inhibitor of aggregation. The log dose‐response relation during ADP aggregation with and without VK 744 suggests that this substance acts as a functional inhibitor.
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Sixma et al. (1971) studied In vitro human blood platelets. VK 744 vs. RA 233 / without VK 744 was evaluated on Platelet aggregation and function. In vitro, VK 744 acts as a functional inhibitor of human blood platelets, inhibiting collagen aggregation at 25 μM and ADP aggregation at 50 μM.
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