Wildt L, Hutchison J S, Marshall G, Pohl C R, Knobil E
Endocrinology. 1981 Oct;109(4):1293-4. doi: 10.1210/endo-109-4-1293.
The site of action of progesterone (P) in the blockade of estradiol-induced gonadotropin discharges was examined in rhesus monkeys bearing hypothalamic lesions which abolish endogenous GnRH production. Normal ovulatory menstrual cycles were re-established in these animals by the pulsatile, hourly administration of GnRH. In the follicular phase of these induced menstrual cycles, P-containing Silastic capsules were implanted sc yielding luteal phase plasma P concentrations which normally block estradiol-induced gonadotropin surges. P failed to block estradiol-induced surges in lesioned animals on GnRH replacement. In such animals, however, P advanced the initiation of these surges. While estradiol acts on the pituitary to cause gonadotropin discharges, P appears to block this effect by acting on the central nervous system. On the other hand, the results also suggest that the site of facilitatory action of P on gonadotropin release is at the level of the pituitary gland.
在切除了能消除内源性促性腺激素释放激素（GnRH）分泌的下丘脑的恒河猴中，研究了孕酮（P）阻断雌二醇诱导的促性腺激素释放的作用位点。通过每小时脉冲式给予GnRH，在这些动物中重新建立了正常的排卵性月经周期。在这些诱导的月经周期的卵泡期，皮下植入含P的硅橡胶胶囊，使血浆P浓度达到黄体期水平，该浓度通常会阻断雌二醇诱导的促性腺激素激增。在接受GnRH替代治疗的损伤动物中，P未能阻断雌二醇诱导的激增。然而，在这类动物中，P提前了这些激增的起始时间。虽然雌二醇作用于垂体导致促性腺激素释放，但P似乎通过作用于中枢神经系统来阻断这种效应。另一方面，结果还表明，P对促性腺激素释放的促进作用位点在垂体水平。
