Maka F D, Breuiller-Fouche M, Geny B, Ferre F
INSERM. U. 361, Reproduction et Physiopathologie Obstetricale, Maternite Baudelocque, Paris, France.
Prostaglandins. 1993 Mar;45(3):269-83. doi: 10.1016/0090-6980(93)90052-9.
We examined the effect of prostaglandin F2 alpha (PGF2 alpha) on phosphoinositide (PI)-hydrolysis in the outer layer of the human myometrium at the end of pregnancy. After pretreatment of myometrial explants with a cyclo-oxygenase inhibitor (indomethacin), the PGF2 alpha dose-response curve was shifted to the left and a maximal level of PGF2 alpha-induced IP accumulation was reached. In contrast, the well-known OT-induced IP accumulation was decreased in the presence of indomethacin, whereas potency was unchanged. Incubation of the myometrial explants with calcium-depleted medium, not only decreased the basal IP production but completely abolished the OT- and PGF2 alpha-induced IP accumulation. A L-type calcium channel inhibitor, verapamil 100 microM, significantly decreased PGF2 alpha-induced total inositol production whereas it had no effect on OT-response, suggesting that the first event of PGF2 alpha action is the activation of a calcium channel. These results point to marked differences in the mechanisms by which OT and PGF2 alpha exert their contractile effects in human myometrium at the end of pregnancy.
我们研究了妊娠末期前列腺素F2α（PGF2α）对人子宫肌层外层磷酸肌醇（PI）水解的影响。在用环氧化酶抑制剂（吲哚美辛）预处理子宫肌层外植体后，PGF2α剂量反应曲线向左移动，达到了PGF2α诱导的肌醇磷酸（IP）积累的最大水平。相反，在吲哚美辛存在的情况下，众所周知的催产素（OT）诱导的IP积累减少，而效力不变。用缺钙培养基培养子宫肌层外植体，不仅降低了基础IP产生，而且完全消除了OT和PGF2α诱导的IP积累。一种L型钙通道抑制剂，100微摩尔的维拉帕米，显著降低了PGF2α诱导的总肌醇产生，而对OT反应没有影响，这表明PGF2α作用的第一个事件是钙通道的激活。这些结果表明，在妊娠末期，OT和PGF2α在人子宫肌层发挥收缩作用的机制存在显著差异。
