Evans P M
Cytobios. 1978;23(90):101-8.
Like ATP the analogue beta, gamma-methylene-ATP (AMP-PCP) is shown to be an inhibitor of both ADP-induced shape change and aggregation of human platelets. The effect of AMP-PCP on aggregation is not dependent on its conversion to adenosine, though in the presence of plasma adenosine is produced and the inhibitory effect is enhanced. Since AMP-PCP cannot be enzymatically cleaved at the beta, gamma-position the inhibitory effect cannot be attributed to utilisation of the analogue by a surface-located ATPase as has been suggested for ATP. Alternative explanations for the effect are considered with respect to some current theories of ADP-induced platelet aggregation.
与三磷酸腺苷（ATP）类似，β，γ-亚甲基三磷酸腺苷（AMP-PCP）被证明是二磷酸腺苷（ADP）诱导的人血小板形态变化和聚集的抑制剂。AMP-PCP对聚集的作用并不依赖于其转化为腺苷，不过在血浆存在的情况下会产生腺苷，且抑制作用会增强。由于AMP-PCP不能在β，γ位被酶切，其抑制作用不能像ATP那样归因于位于表面的ATP酶对该类似物的利用。关于ADP诱导血小板聚集的一些当前理论，对该作用的其他解释也在考虑之中。
