Goureau O, Tanfin Z, Marc S, Harbon S
Laboratoire d'Endocrinologie et Régulations Cellulaires, Centre National de la Recherche Scientifique URA 1131, Université Paris Sud, Orsay, France.
Am J Physiol. 1992 Jul;263(1 Pt 1):C257-65. doi: 10.1152/ajpcell.1992.263.1.C257.
Attempts were made to identify prostaglandin (PG) receptors in rat myometrium, according to the differential rank order of potencies displayed by the natural PGs and their analogues, both at the level of second messenger generation and contraction. In estrogen-treated rat myometrium, PGs [iloprost = PGI2 greater than PGE2 much greater than 16,16-dimethyl (DM)-PGE2; sulprostone = misoprostol = 0] induced adenosine 3',5'-cyclic monophosphate generation, indicating the contribution of a PGI2 receptor. The generation of inositol phosphates was stimulated by PGs (PGF2 alpha greater than PGD2 much greater than PGE2 = DM-PGE2 much greater than iloprost greater than sulprostone = misoprostol = 0), reflecting a PGF2 alpha-receptor-mediated process, which was insensitive to pertussis toxin (PTX). Contractions caused by PGF2 alpha were closely correlated to PGF2 alpha-receptor activation associated with the phospholipase C pathway. By contrast, contractions evoked by PGE2, equally mimicked by sulprostone and misoprostol, were abolished by PTX and were independent of phospholipase C activation. In the pregnant myometrium (day 21), the latter PGE-receptor-mediated mechanism also contributed to contractions caused by PGE2 (less than microM concn). Phospholipase C activation was coupled not only to PGF2 alpha but also to PGE receptors and could be correlated with contractions induced by PGF2 alpha and PGE2 greater than microM concn). All PGs tested were coupled to inhibitory G protein-mediated adenylate cyclase inhibition, displaying an equipotency that did not allow characterization of the inhibitory PG receptors.
根据天然前列腺素（PG）及其类似物在第二信使生成和收缩水平上显示的效价差异顺序，人们试图鉴定大鼠子宫肌层中的PG受体。在雌激素处理的大鼠子宫肌层中，PGs[依洛前列素=前列环素I2大于前列腺素E2远大于16,16-二甲基（DM）-前列腺素E2；舒前列素=米索前列醇=0]诱导3',5'-环磷酸腺苷生成，表明存在前列环素I2受体。PGs（前列腺素F2α大于前列腺素D2远大于前列腺素E2=DM-前列腺素E2远大于依洛前列素大于舒前列素=米索前列醇=0）刺激肌醇磷酸生成，反映了由前列腺素F2α受体介导的过程，该过程对百日咳毒素（PTX）不敏感。前列腺素F2α引起的收缩与磷脂酶C途径相关的前列腺素F2α受体激活密切相关。相比之下，前列腺素E2引起的收缩，舒前列素和米索前列醇同样能模拟，可被PTX消除且与磷脂酶C激活无关。在妊娠子宫肌层（第21天），后一种前列腺素E受体介导的机制也促成了由前列腺素E2（浓度小于微摩尔）引起的收缩。磷脂酶C激活不仅与前列腺素F2α相关，还与前列腺素E受体相关，并且可能与大于微摩尔浓度的前列腺素F2α和前列腺素E2诱导的收缩相关。所有测试的PGs均与抑制性G蛋白介导的腺苷酸环化酶抑制相关，其效价相同，无法区分抑制性PG受体。
