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  • Title: Decrease of platelet aggregation and spreading via inhibition of the cAMP phosphodiesterase by trapidil.
    Author: Mazurov AV, Menshikov MYu, Leytin VL, Tkachuk VA, Repin VS.
    Journal: FEBS Lett; 1984 Jul 09; 172(2):167-71. PubMed ID: 6086387.
    Abstract:
    Trapidil (N,N-diethyl-5-methyl[1,2,4]triazolo[1,5-alpha]pyrimidine-7-amine ) inhibits platelet spreading and aggregation induced by arachidonic acid (AA), a stable analogue of prostaglandin (PG) endoperoxides (U46619), ADP, and low concentrations of thrombin, but not by A23187 and high concentrations of thrombin. Trapidil does not affect platelet adenylate cyclase but inhibits the cAMP PDE by approx. 50%. PDE inhibition proceeds via a competitive mechanism (Ki = 0.52 mM) and is not mediated by calmodulin inhibition. Trapidil does not change the platelet basal cAMP level but potentiates an increase of cAMP induced by the stable prostacyclin analogue (6 beta-PGI1). These results suggest that trapidil antiplatelet effects may be due to the inhibition of platelet PDE.
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