Perusquia M, Kubli-Garfias C
Unidad de Investigacion Biomedica, IMSS, Mexico City, Mexico.
Prostaglandins. 1992 May;43(5):445-55. doi: 10.1016/0090-6980(92)90127-f.
Prostaglandins (PGs) E2 and F2 alpha are strong inducers of uterine contraction by promoting a Ca2+ increase into the cell through specific receptors coupled with the calcium channels. On the contrary, progesterone and 5 beta-reduced progestins promote smooth muscle relaxation by blocking the ion calcium influx. Thus, this study was designed to emphasize the importance of external calcium in the PGs-induced rat uterus contraction. Likewise, also studied was the antagonism and the interaction between PGs and progestins (progesterone and its 5 alpha and 5 beta-reduced derivatives) in the myometrium. Results showed that uterine contraction induced by PGs depends on external calcium, since verapamil or extracellular calcium depletion abolished the PGs effect. Regarding the PGs-progestins antagonism, it was observed that pregnanedione, pregnanolone and epipregnanolone were quite effective for counteracting of PGs-induced contraction. However, progesterone was effective in a middle range, whereas 5 alpha-reduced progestins (allopregnanedione and allopregnanolone) were almost ineffective. It has been concluded that the participation of PGs and progestins in the modulation of uterine contraction might be achieved through the control of calcium influx by opening (PGs) or blocking (progestins) receptor-operated calcium channels.
前列腺素（PGs）E2和F2α是子宫收缩的强诱导剂，它们通过与钙通道偶联的特定受体促进钙离子进入细胞，从而增加细胞内钙离子浓度。相反，孕酮和5β-还原孕激素通过阻止钙离子内流来促进平滑肌松弛。因此，本研究旨在强调细胞外钙在PGs诱导的大鼠子宫收缩中的重要性。同样，还研究了PGs与孕激素（孕酮及其5α和5β-还原衍生物）在子宫肌层中的拮抗作用和相互作用。结果表明，PGs诱导的子宫收缩依赖于细胞外钙，因为维拉帕米或细胞外钙耗竭可消除PGs的作用。关于PGs与孕激素的拮抗作用，观察到孕烷二酮、孕烷醇酮和表孕烷醇酮对抵消PGs诱导的收缩相当有效。然而，孕酮在中等剂量时有效，而5α-还原孕激素（别孕烷二酮和别孕烷醇酮）几乎无效。得出的结论是，PGs和孕激素参与子宫收缩调节可能是通过打开（PGs）或阻断（孕激素）受体操纵的钙通道来控制钙离子内流实现的。
