Cusack N J, Hourani S M
Br J Pharmacol. 1982 Feb;75(2):257-9. doi: 10.1111/j.1476-5381.1982.tb08781.x.
Adenosine 5'-diphosphate (ADP) induces human platelet aggregation and inhibits stimulated adenylate cyclase. Adenosine 5'-O-(1-thiodiphosphate) (ADP-alpha-S) and adenosine 5'-O-(2-thiodiphosphate) (ADP-beta-S) act at the ADP receptor and achieve the same maximal rate of human platelet aggregation as each other. Adenosine and prostaglandin E1, which noncompetitively inhibit ADP-induced aggregation by stimulating adenylate cyclase, inhibit aggregation induced by ADP-x-S more than aggregation induced by ADP-beta-S. ADP-x-S, unlike ADP-beta-S and ADP itself, does not inhibit stimulated adenylate cyclase. This suggests that the inhibition of stimulated adenylate cyclase by ADP, although not a cause of aggregation, may be of physiological importance in reducing the effects of endogenous agents such as adenosine and prostaglandins (for example, prostacyclin) to which the platelet may be exposed.
5'-二磷酸腺苷(ADP)可诱导人血小板聚集,并抑制受刺激的腺苷酸环化酶。5'-O-(1-硫代二磷酸)腺苷(ADP-α-S)和5'-O-(2-硫代二磷酸)腺苷(ADP-β-S)作用于ADP受体,且彼此达到相同的人血小板最大聚集速率。腺苷和前列腺素E1通过刺激腺苷酸环化酶非竞争性抑制ADP诱导的聚集,它们对ADP-α-S诱导的聚集的抑制作用比对ADP-β-S诱导的聚集的抑制作用更强。与ADP-β-S和ADP本身不同,ADP-α-S不抑制受刺激的腺苷酸环化酶。这表明,ADP对受刺激的腺苷酸环化酶的抑制作用虽然不是聚集的原因,但在减轻血小板可能接触到的内源性物质(如腺苷和前列腺素,例如前列环素)的影响方面可能具有生理重要性。