A SUPPRESSION OF GONADOTROPIN-SECRETION BY CORTISOL IN CASTRATED MALE RHESUS-MONKEYS (MACACA-MULATTA) MEDIATED BY THE INTERRUPTION OF HYPOTHALAMIC GONADOTROPIN-RELEASING HORMONE-RELEASE

A SUPPRESSION OF GONADOTROPIN-SECRETION BY CORTISOL IN CASTRATED MALE RHESUS-MONKEYS (MACACA-MULATTA) MEDIATED BY THE INTERRUPTION OF HYPOTHALAMIC GONADOTROPIN-RELEASING HORMONE-RELEASE
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DOI:
10.1095/biolreprod33.2.423
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发表时间:
1985-01-01
影响因子:
3.6
通讯作者:
PLANT, TM
PLANT, TM
中科院分区:
生物学2区
文献类型:
--
作者:
DUBEY, AK;PLANT, TM

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对4只3~3.5岁的去恒河猴进行了62天的每日肌注治疗。注射醋酸氢化可的松(HCA),剂量为10-20毫克/(公斤体重)。每天或每隔一天在治疗前、治疗中和治疗后采集血样。注射醋酸氢化可的松导致平均血浆皮质醇浓度从激素治疗开始前的基础浓度17-35微克/100毫升逐渐上升到5周后的约150微克/100毫升。当血清皮质醇浓度在HCA治疗开始后3-4wk达到100ug/100ml时,循环黄体生成素(LH)和卵泡刺激素(FSH)开始下降,35天后达到检测不到的浓度。停用HCA后,血浆皮质醇浓度恢复到治疗前对照水平,这与促性腺激素分泌完全恢复有关。在2只动物中,间歇静脉注射。静脉输注促性腺激素释放激素(GnRH)(0.1ug/min,每小时一次,每次3min),似乎以生理方式刺激促性腺激素,逆转皮质醇对促性腺激素分泌的抑制,使循环中的促黄体生成素和卵泡刺激素浓度恢复到对照组的80%-100%。这些结果表明,在恒河猴中,皮质醇对促性腺激素释放的抑制作用主要位于甲状腺上水平,并通过阻断下丘脑GnRH的释放而起作用。
Four orchidectomized rhesus monkeys (3-3.5 yr of age) were treated for 62 days with daily i.m. injections of hydrocortisone acetate (HCA) at a dose of 10-20 mg/(kg BW .cntdot. day), and blood samples were obtained daily or every other day before, during and after treatment. Hydrocortisone acetate injections resulted in a progressive rise in mean plasma cortisol from basal concentrations of 17-35 .mu.g/100 ml prior to initiation of steroid treatment to approximately 150 .mu.g/100 ml 5 wk later. When serum cortisol concentrations reached 100 .mu.g/100 ml, 3-4 wk after the initiation of HCA treatment, circulating luteinizing hormone (LH) and follicle-stimulating hormone (FSH) began to decline, reaching nondetectable concentrations 35 days later. Withdrawal of HCA resulted in a return in plasma cortisol concentrations to pretreatment control levels, which was associated with a complete restoration of gonadotropin secretion. In 2 animals, administration of an intermittent i.v. infusion of gonadotropin-releasing hormone (GnRH) (0.1 .mu.g/min for 3 min once every hour), which appears to stimulate the gonadotropes in a physiologic manner, reversed the cortisol-induced inhibition of gonadotropin secretion, restoring circulating LH and FSH concentrations to within 80-100% of control. These results suggest that, in the rhesus monkey, the major site of the inhibitory action of cortisol on gonadotropin release resides at a suprapituitary level and is mediated by interruption of hypothalamic GnRH release.