Marshall J C, Griffin M L
Department of Internal Medicine, University of Virginia Health Sciences Center, Charlottesville 22908.
Hum Reprod. 1993 Nov;8 Suppl 2:57-61. doi: 10.1093/humrep/8.suppl_2.57.
Ovulatory cycles in women result from sequential stimulation of ovarian follicular development by pituitary follicle stimulating hormone (FSH) and luteinizing hormone (LH). In the follicular phase the initial FSH stimulus declines and LH secretion increases toward the mid-cycle ovulatory surge. During the luteal phase gonadotrophin secretion is reduced. This reflects the effects of ovarian steroids inhibiting the frequency of gonadotrophin releasing hormone (GnRH) secretion by the hypothalamus, and the direct effects of oestradiol and inhibin to reduce gonadotroph (FSH) secretion. The frequency of GnRH stimulation of the gonadotroph is a selective regulator of gonadotrophin synthesis, with slow frequency stimuli favouring FSH and faster frequency stimuli favouring LH secretion. Current research has only revealed a single gonadotrophin releasing hormone. Thus, the ability to change the pattern (particularly frequency) of GnRH stimulation of the gonadotroph is proposed as an important regulator of differential FSH and LH synthesis, and hence of ovulatory cycles. In some disorders of ovulation the ability to regulate GnRH pulse frequency appears to have been lost. Slow frequency GnRH pulses are consistently seen in women with hypothalamic amenorrhoea and hyperprolactinaemia. The reduced GnRH secretion appears to reflect increased hypothalamic opiate tone and can be rapidly reversed with an opiate receptor blocker. Other disorders associated with anovulation show rapid frequency GnRH secretion, and polycystic ovarian syndrome (PCO) is commonly associated with fast-frequency, high-amplitude LH (GnRH) pulses. Such a GnRH stimulus would favour LH and androgen production and the failure of ovarian follicular maturation in PCO may reflect inappropriate sequential FSH secretion.(ABSTRACT TRUNCATED AT 250 WORDS)
女性的排卵周期是由垂体促卵泡激素（FSH）和促黄体生成素（LH）对卵巢卵泡发育的顺序刺激所致。在卵泡期，最初的FSH刺激减弱，LH分泌在周期中期排卵高峰前增加。在黄体期，促性腺激素分泌减少。这反映了卵巢类固醇抑制下丘脑促性腺激素释放激素（GnRH）分泌频率的作用，以及雌二醇和抑制素直接减少促性腺激素（FSH）分泌的作用。GnRH对促性腺激素的刺激频率是促性腺激素合成的选择性调节因子，低频刺激有利于FSH分泌，高频刺激有利于LH分泌。目前的研究仅发现了一种促性腺激素释放激素。因此，改变GnRH对促性腺激素刺激模式（特别是频率）的能力被认为是FSH和LH合成差异以及排卵周期的重要调节因子。在一些排卵障碍中，调节GnRH脉冲频率的能力似乎丧失了。在下丘脑性闭经和高催乳素血症的女性中持续可见低频GnRH脉冲。GnRH分泌减少似乎反映了下丘脑阿片样物质张力增加，使用阿片受体阻滞剂可迅速逆转。与无排卵相关的其他疾病表现为GnRH快速分泌，多囊卵巢综合征（PCO）通常与高频、高幅度LH（GnRH）脉冲有关。这种GnRH刺激有利于LH和雄激素的产生，PCO中卵巢卵泡成熟失败可能反映了FSH分泌顺序不当。（摘要截选至250词）
