Benigni A, Livio M, Dodesini P, Schieppati A, Panigada M, Mecca G, de Gaetano G, Remuzzi G
Am J Nephrol. 1985;5(4):243-7. doi: 10.1159/000166942.
Parathyroid hormone (PTH) is a polypeptide which in different in vitro systems raises intracellular cyclic AMP (cAMP) levels via adenyl cyclase activation and stimulates Ca2+ transport across cell membranes. We tested whether, on the basis of this mechanism, PTH would inhibit human platelet aggregation. The latter was tested in vitro by a photometric technique. Platelet aggregation induced by the calcium ionophore A 23187 was inhibited by PTH at concentrations (0.5-3 USP U/ml) similar to those effective in other in vitro systems. Higher concentrations of PTH were required to prevent aggregation initiated by adenosine-5'-diphosphate, arachidonic acid, or platelet-aggregating factor. The terminal synthetic fragment 1-34 b PTH was ineffective against all aggregation stimuli. The antiaggregating effect of PTH was potentiated by verapamil and theophylline and was additive to that of PGI2. However, PTH did not appear to increase platelet cAMP levels and was not counteracted by an inhibitor of platelet adenyl cyclase. It is therefore unlikely that PTH inhibits platelet aggregation through an adenyl cyclase stimulated increase of cAMP. Since PTH levels are markedly increased in uremic plasma, it might contribute to the defective platelet function and the bleeding tendency frequently occurring in uremic patients.
甲状旁腺激素（PTH）是一种多肽，在不同的体外系统中，它通过激活腺苷酸环化酶提高细胞内环磷酸腺苷（cAMP）水平，并刺激钙离子跨细胞膜转运。我们基于这一机制测试了PTH是否会抑制人血小板聚集。后者通过光度技术在体外进行测试。钙离子载体A 23187诱导的血小板聚集在浓度（0.5 - 3 USP U/ml）下被PTH抑制，该浓度与在其他体外系统中有效的浓度相似。需要更高浓度的PTH来防止由腺苷 - 5'-二磷酸、花生四烯酸或血小板聚集因子引发的聚集。PTH的末端合成片段1 - 34对所有聚集刺激均无效。维拉帕米和茶碱可增强PTH的抗聚集作用，且其作用与前列环素（PGI2）的作用相加。然而，PTH似乎并未增加血小板cAMP水平，也未被血小板腺苷酸环化酶抑制剂所拮抗。因此，PTH不太可能通过腺苷酸环化酶刺激cAMP增加来抑制血小板聚集。由于尿毒症患者血浆中PTH水平显著升高，它可能导致尿毒症患者常见的血小板功能缺陷和出血倾向。
