Effects of hyperprolactinemia on the control of luteinizing hormone and follicle-stimulating hormone secretion in the male rat.
Effects of hyperprolactinemia on the control of luteinizing hormone and follicle-stimulating hormone secretion in the male rat.
复制标题
高催乳素血症对雄性大鼠黄体生成素和卵泡刺激素分泌控制的影响。
DOI：
10.1095/biolreprod36.1.138
复制
发表时间：
1987
影响因子：
3.6
通讯作者：
Bartke,A
中科院分区：
文献类型：
--
作者：
Smith,MS;Bartke,A
本实验观察了急性高催乳素血症（hyperPRL）对雄性大鼠促黄体生成素（LH）和促卵泡激素（FSH）分泌的影响。从去势时开始暴露于高水平的催乳素（1 mg绵羊催乳素，每日2次），极大地减弱了去势后3天观察到的LH去势后升高。去势后7天，泌乳素处理动物中的LH浓度接近对照动物中观察到的水平。HyperPRL对去势后FSH升高无影响。通过LH对静脉推注25 ng GnRH的反应评估，PPR对促性腺激素释放激素（GnRH）的反应性在去势后3天和7天时仅受到hperPRL的最小影响。对照组和催乳素给药组动物在GnRH后所有时间点的LH反应均相似，但催乳素给药组动物的LH反应峰值显著较小。通过将雄性大鼠离体半垂体暴露于GnRH（5 ng/ml）脉冲（每30 min 6 min），持续4 h，进一步检查hyperPRL的作用。HyperPRL对体外基础LH释放、GnRH刺激的LH释放或完整、去势后3天或去势后7天动物半垂体中的垂体LH浓度无影响。然而，净促性腺激素释放激素刺激的FSH显着较高的垂体高泌乳素血症，去势男性。为了间接评估hyperPRL对GnRH释放的影响，雄性动物在去势后3天接受弓状核/正中隆起（ARC/ME）的电刺激。催乳素水平升高不仅抑制基础LH分泌，而且与对照去势雄性动物的LH反应相比，对电刺激的LH反应降低了50%。这些结果表明，急性高PRL抑制LH分泌，但不FSH分泌。虽然垂体反应性在高催乳素血症男性中有所减弱，但在体内评估时，当垂体在体外暴露于足够量的GnRH时，这是正常的。因此，高PRL对垂体反应性的影响似乎是最小的，特别是如果垂体暴露于足够的GnRH刺激。体内基础LH分泌的抑制很可能反映了内源性GnRH分泌不足。暴露于催乳素的高泌乳素血症男性在电刺激后LH反应大大降低，进一步表明高PRL抑制GnRH分泌。
Experiments were conducted to determine the effects of acute hyperprolactinemia (hyperPRL) on the control of luteinizing hormone and follicle-stimulating hormone secretion in male rats. Exposure to elevated levels of prolactin from the time of castration (1 mg ovine prolactin 2 × daily) greatly attenuated the post-castration rise in LH observed 3 days after castration. By 7 days after castration, LH concentrations in the prolactin-treated animals approached the levels observed in control animals. HyperPRL had no effect on the postcastration rise in FSH. Pituitary responsiveness to gonadotropin hormone-releasing hormone (GnRH), as assessed by LH responses to an i.v. bolus of 25 ng GnRH, was only minimally effected by hperPRL at 3 and 7 days postcastration. LH responses were similar at all time points after GnRH in control and prolactin-treated animals, except for the peak LH responses, which were significantly smaller in the prolactin-treated animals. The effects of hyperPRL were examined further by exposing hemipituitaries in vitro from male rats to 6-min pulses of GnRH (5 ng/ml) every 30 min for 4 h. HyperPRL had no effect on basal LH release in vitro, on GnRH-stimulated LH release, or on pituitary LH concentrations in hemipituitaries from animals that were intact, 3 days postcastration, or 7 days postcastration. However, net GnRH-stimulated release of FSH was significantly higher by pituitaries from hyperprolactinemic, castrated males. To assess indirectly the effects of hyperPRL on GnRH release, males were subjected to electrical stimulation of the arcuate nucleus/median eminence (ARC/ME) 3 days postcastration. The presence of elevated levels of prolactin not only suppressed basal LH secretion but reduced the LH responses to electrical stimulation by 50% when compared to the LH responses in control castrated males. These results suggest that acute hyperPRL suppresses LH secretion but not FSH secretion. Although pituitary responsiveness is somewhat attenuated in hyperprolactinemic males, as assessed in vivo, it is normal when pituitaries are exposed to adequate amounts of GnRH in vitro. Thus, the effects of hyperPRL on pituitary responsiveness appear to be minimal, especially if the pituitary is exposed to an adequate GnRH stimulus. The suppression of basal LH secretion in vivo most likely reflects inadequate endogenous GnRH secretion. The greatly reduced LH responses after electrical stimulation in hyperprolactinemic males exposed to prolactin suggest further that hyperPRL suppresses GnRH secretion.