Mazurov A V, Leytin V L, Tkachuk V A, Repin V S
FEBS Lett. 1984 Jul 9;172(2):167-71. doi: 10.1016/0014-5793(84)81119-9.
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.
曲匹地尔（N，N - 二乙基 - 5 - 甲基[1,2,4]三唑并[1,5 - α]嘧啶 - 7 - 胺）可抑制由花生四烯酸（AA）、前列腺素（PG）内过氧化物的稳定类似物（U46619）、二磷酸腺苷（ADP）和低浓度凝血酶诱导的血小板铺展和聚集，但对离子载体A23187和高浓度凝血酶诱导的血小板铺展和聚集无抑制作用。曲匹地尔不影响血小板腺苷酸环化酶，但可抑制环磷酸腺苷磷酸二酯酶（cAMP PDE）约50%。磷酸二酯酶的抑制通过竞争机制进行（抑制常数Ki = 0.52 mM），且不受钙调蛋白抑制的介导。曲匹地尔不改变血小板基础环磷酸腺苷（cAMP）水平，但可增强稳定前列环素类似物（6β - PGI1）诱导的cAMP升高。这些结果表明，曲匹地尔的抗血小板作用可能归因于对血小板磷酸二酯酶的抑制。
