前列腺素内过氧化物在体外可促进血小板膜组分释放钙。

Prostaglandin endoperoxides promote calcium release from a platelet membrane fraction in vitro.

作者信息

Gerrard J M, Butler A M, Graff G, Stoddard S F, White J G

出版信息

Prostaglandins Med. 1978 Nov;1(5):373-85. doi: 10.1016/0161-4630(78)90124-6.

Abstract

A calcium sequestering platelet membrane fraction was prepared and the effect of arachidonic acid, PGG2 and PGH2 on calcium content evaluated. At 4 degrees C, 6.7--16.7 micrometers arachidonic acid caused significant release of calcium from preloaded vesicles. Such release was completely inhibited by aspirin pretreating the platelets from which the membrane fraction was prepared. Gamma-linolenic acid, not a substrate for prostaglandin synthesis, did not cause calcium release. At 37 degrees C, after a 5 minute calcium loading of the membrane vesicles, arachidonic acid, PGG2, and PGH2 caused release of calcium. Calcium release by the PGG2 and PGH2 was only slightly inhibited by aspirin. Imidazole, which prevented conversion of the prostaglandin endoperoxides to thromboxanes, also only slightly inhibited calcium release. Other prostaglandins including PGD2, PGE1, PGE2 and PGD2 had no effect on the calcium content of the vesicles. These studies suggest that PGG2 and PGH2 may exert their effects on platelets by mobilizing calcium from an internal membrane store to make it available to promote platelet activation.

摘要

制备了一种钙隔离血小板膜组分，并评估了花生四烯酸、前列腺素G2（PGG2）和前列腺素H2（PGH2）对钙含量的影响。在4℃时，6.7 - 16.7微米的花生四烯酸导致预加载囊泡中的钙显著释放。这种释放被阿司匹林预处理制备膜组分所用的血小板完全抑制。γ-亚麻酸不是前列腺素合成的底物，不会引起钙释放。在37℃时，膜囊泡钙加载5分钟后，花生四烯酸、PGG2和PGH2导致钙释放。PGG2和PGH2引起的钙释放仅被阿司匹林轻微抑制。咪唑可阻止前列腺素内过氧化物转化为血栓素，它也仅轻微抑制钙释放。其他前列腺素，包括前列腺素D2（PGD2）、前列腺素E1（PGE1）、前列腺素E2（PGE2）和PGD2对囊泡的钙含量没有影响。这些研究表明，PGG2和PGH2可能通过从内膜储存中动员钙来发挥其对血小板的作用，使其可用于促进血小板活化。