Progesterone blocks the estradiol-induced gonadotropin discharge in the ewe by inhibiting the surge of gonadotropin-releasing hormone.
Progesterone blocks the estradiol-induced gonadotropin discharge in the ewe by inhibiting the surge of gonadotropin-releasing hormone.
复制标题
DOI：
10.1210/endo.131.1.1611998
复制
发表时间：
1992-07
期刊：
影响因子：
4.8
通讯作者：
J. Z. Kasa-Vubu;G E Dahl;N. P. Evans;L. Thrun;S. Moenter;Vasantha Padmanabhan;F. Karsch
中科院分区：
文献类型：
--
作者：
J. Z. Kasa-Vubu;G E Dahl;N. P. Evans;L. Thrun;S. Moenter;Vasantha Padmanabhan;F. Karsch
先前的研究表明，循环孕酮的升高阻断了循环雌二醇升高的正反馈效应。这解释了为什么在月经或发情周期的黄体期没有促性腺激素激增，尽管循环中的雌二醇偶尔会上升到足以引起激增的浓度。最近的研究表明，雌二醇通过诱导GnRH分泌大量激增，在垂体门脉脉管系统中可测量，从而引发羊体内LH激增。我们验证了黄体酮通过阻止GnRH激增来阻断雌二醇诱导的羊体内LH和FSH激增的假设。成年萨福克母羊被切除卵巢，用硅橡胶植入来产生和维持黄体中期循环雌二醇和黄体酮的浓度，并通过手术安装一个装置来采集垂体门静脉血液。一周后，母羊被分为两组：一组是激波诱导组（n = 5），其中移除孕酮植入物以模拟黄体溶解，另一组是激波阻断组（n = 5），接受假植入物移除，以维持孕酮的升高。在去除黄体酮植入物（或假植入物）16小时后，所有动物都接受额外的雌二醇植入物治疗，以使循环雌二醇增加，如在发情周期的卵泡期所见。每小时采集垂体门脉血和颈静脉血24小时，跨越预期激素激增的时间，之后静脉注射GnRH，以测试垂体对释放激素的反应。激波诱导组的所有动物均表现出GnRH、LH和FSH的剧烈激波，但在促性腺激素激波终止后的数小时内，促性腺激素的分泌并未因GnRH的刺激而增加。在所有维持孕酮水平升高的动物中，GnRH、LH和FSH的激增都被阻断。然而，激波阻滞组的这些动物确实分泌了LH来应对GnRH的挑战。我们得出结论，黄体酮阻断雌二醇诱导的促性腺激素在母羊体内的释放，通过中枢作用抑制分泌到垂体门静脉血管的GnRH的激增。
Previous studies indicate an elevation of circulating progesterone blocks the positive feedback effect of a rise in circulating estradiol. This explains the absence of gonadotropin surges in the luteal phase of the menstrual or estrous cycle despite occasional rises in circulating estradiol to a concentration sufficient for surge induction. Recent studies demonstrate estradiol initiates the LH surge in sheep by inducing a large surge of GnRH secretion, measurable in the hypophyseal portal vasculature. We tested the hypothesis that progesterone blocks the estradiol-induced surge of LH and FSH in sheep by preventing this GnRH surge. Adult Suffolk ewes were ovariectomized, treated with Silastic implants to produce and maintain midluteal phase concentrations of circulating estradiol and progesterone, and an apparatus was surgically installed for sampling of pituitary portal blood. One week later the ewes were allocated to two groups: a surge-induction group (n = 5) in which the progesterone implants were removed to simulate luteolysis, and a surge-block group (n = 5) subjected to a sham implant removal such that the elevation in progesterone was maintained. Sixteen hours after progesterone-implant removal (or sham removal), all animals were treated with additional estradiol implants to produce a rise in circulating estradiol as seen in the follicular phase of the estrous cycle. Hourly samples of pituitary portal and jugular blood were obtained for 24 h, spanning the time of the expected hormone surges, after which an iv bolus of GnRH was injected to test for pituitary responsiveness to the releasing hormone. All animals in the surge-induction group exhibited vigorous surges of GnRH, LH, and FSH, but failed to show a rise in gonadotropin secretion in response to the GnRH challenge given within hours of termination of the gonadotropin surges. The surges of GnRH, LH, and FSH were blocked in all animals in which elevated levels of progesterone were maintained. These animals in the surge-block group, however, did secrete LH in response to the GnRH challenge. We conclude progesterone blocks the estradiol-induced gonadotropin discharge in the ewe by acting centrally to inhibit the surge of GnRH secreted into the hypophyseal portal vasculature.