促肾上腺皮质激素对体外促性腺激素释放激素诱导的黄体生成素分泌的影响。
Effect of adrenocorticotrophic hormone on gonadotrophin releasing hormone-induced luteinizing hormone secretion in vitro.
作者信息
Phogat J B, Smith R F, Dobson H
机构信息
Department of Veterinary Clinical Science and Animal Husbandry, University of Liverpool, Neston, South Wirral, UK.
出版信息
Anim Reprod Sci. 1997 Jul;48(1):53-65. doi: 10.1016/s0378-4320(97)00030-4.
An in vitro perifusion study investigated the effect of different forms of adrenocorticotrophic hormone (ACTH) on gonadotrophin releasing hormone (GnRH)-induced luteinizing hormone (LH) secretion, particularly GnRH self-priming, and oestradiol sensitisation of the ovine pituitary. Fragments of pituitaries were obtained from mixed-breed adult nonpregnant female sheep (without corpora lutea, unless otherwise stated). The amount of LH released by different doses of GnRH (2.5 x 10(-10) M (n = 9 chambers), 1 x 10(-10) M (n = 9), or 5 x 10(-11) M (n = 6)) was evaluated by giving two GnRH pulses (5 min each) 2 h apart. In a duplicate set of chambers, ACTH1-24 (5 x 10(-7) M) was included in the perifusate 0.5 h before the first GnRH challenge. Potassium chloride (KCl; 100 mM) was administered 2 h after the second GnRH challenge to assess the viability of the tissue and the size of the releasable LH pool. Results were expressed as percentage of LH secretion. The influence of ACTH1-24 on oestradiol sensitisation was also examined using pituitaries obtained during the luteal phase. Pituitary tissues were perifused throughout with 1 x 10(-9) M or 6 x 10(-11) M oestradiol in the medium. The LH response to the second GnRH challenge (GnRH 2) was significantly greater (p < 0.01) than after the first (GnRH 1) at the highest dose of GnRH (2.5 x 10(-10) M; 2547 +/- 804 vs. 4547 +/- 1013%), but at the lower doses (1 x 10(-10) M or 5 x 10(-11) M), the self-priming effect of GnRH was not evident (3016 +/- 550 vs. 2932 +/- 490% and 841 +/- 205 vs. 711 +/- 87%). Treatment with ACTH1-24 (5 x 10(-7) M) did not affect tonic LH secretion nor the LH response to the first or second GnRH challenge at any of the GnRH doses tested. The LH released in response to KCl was also similar from control and ACTH1-24-treated tissue at all GnRH doses. Both lower doses of GnRH (1 x 10(-10) M or 5 x 10(-11) M) produced the self-priming effect when the pituitary tissue was sensitised with the higher dose of oestradiol (1 x 10(-9) M; 1711 +/- 239 vs. 5085 +/- 1307%, and 1502 +/- 376 vs. 2619 +/- 629%). In the presence of lower concentrations of oestradiol (6 x 10(-11) M), self-priming was observed only after the higher dose of GnRH (1 x 10(-10) M; 1293 +/- 214 vs. 2865 +/- 436%), not the lower dose (5 x 10(-11) M; 985 +/- 203 vs. 1271 +/- 436%). In spite of these differences, ACTH1-24 treatment did not affect LH secretion (neither basal nor potassium-induced). The effect of ACTH1-39 (1 x 10(-8) M or 5 x 10(-7) M; n = 6 chambers per combination) on GnRH-induced LH secretion was examined using the higher (2.5 x 10(-10) M) or lower dose of GnRH (1 x 10(-10) M), with or without oestradiol sensitisation (1 x 10(-9) M). At the lower dose (1 x 10(-8) M), ACTH1-39 influenced neither tonic nor GnRH-induced LH secretion. The LH released by KCl was also similar to the control and ACTH-treated tissue. In contrast, the higher dose of ACTH1-39 (5 x 10(-7) M) increased tonic LH secretion immediately after inclusion in the medium (104 +/- 3 vs. 161 +/- 20%), but suppressed the GnRH self-priming effect after 2.5 x 10(-10) M, i.e., the LH responses to GnRH 1 and 2 were similar (1786 +/- 294 vs. 1553 +/- 373%). However, the LH response to KCl was not significantly different (p > 0.05) between the control and ACTH-treated tissues (2333 +/- 286 vs. 2638 +/- 431%). When the effect of this higher dose of ACTH1-39 on oestradiol-priming was investigated, ACTH increased tonic LH secretion but suppressed the self-priming effect of GnRH (1 x 10(-10) M GnRH; 945 +/- 274 vs. 922 +/- 323%; p > 0.05), and decreased (p < 0.05) the LH released in response to KCl compared to the controls (1803 +/- 409 vs. 4302 +/- 1017%). In summary, in vitro, ACTH1-24 did not affect either tonic LH secretion, the GnRH self-priming effect, or oestradiol sensitisation. The entire ACTH1-39 increased tonic LH secretion, but reduced GnRH self-priming and oestradiol sensitisation. (ABSTRACT TRUNCATED)
一项体外灌流研究调查了不同形式的促肾上腺皮质激素（ACTH）对促性腺激素释放激素（GnRH）诱导的黄体生成素（LH）分泌的影响，特别是GnRH自身预激发以及绵羊垂体对雌二醇的敏感性。垂体碎片取自成年非妊娠混种母羊（除非另有说明，均无黄体）。通过间隔2小时给予两个GnRH脉冲（每个脉冲5分钟），评估不同剂量的GnRH（2.5×10⁻¹⁰ M（n = 9个小室）、1×10⁻¹⁰ M（n = 9）或5×10⁻¹¹ M（n = 6））释放的LH量。在另一组重复的小室中，在第一次GnRH刺激前0.5小时，将ACTH1 - 24（5×10⁻⁷ M）加入灌流液中。在第二次GnRH刺激后2小时给予氯化钾（KCl；100 mM），以评估组织的活力和可释放LH池的大小。结果以LH分泌的百分比表示。还使用黄体期获得的垂体检查了ACTH1 - 24对雌二醇敏感性的影响。垂体组织在整个过程中用培养基中的1×10⁻⁹ M或6×10⁻¹¹ M雌二醇进行灌流。在最高剂量的GnRH（2.5×10⁻¹⁰ M）时，对第二次GnRH刺激（GnRH 2）的LH反应显著大于第一次（GnRH 1）（p < 0.01；2547±804对4547±1013%），但在较低剂量（1×10⁻¹⁰ M或5×10⁻¹¹ M）时，GnRH的自身预激发效应不明显（3016±550对2932±490%以及841±205对711±87%）。在任何测试的GnRH剂量下，用ACTH1 - 24（5×10⁻⁷ M）处理均不影响LH的基础分泌，也不影响对第一次或第二次GnRH刺激的LH反应。在所有GnRH剂量下，对照组织和经ACTH1 - 24处理的组织对KCl反应释放的LH也相似。当垂体组织用较高剂量的雌二醇（1×10⁻⁹ M）致敏时，两种较低剂量的GnRH（1×10⁻¹⁰ M或5×10⁻¹¹ M）均产生自身预激发效应（1711±239对5085±1307%，以及1502±376对2619±629%）。在较低浓度的雌二醇（6×10⁻¹¹ M）存在下，仅在较高剂量的GnRH（1×10⁻¹⁰ M）后观察到自身预激发（1293±214对2865±436%），较低剂量（5×10⁻¹¹ M）时未观察到（985±203对1271±436%）。尽管存在这些差异，但ACTH1 - 24处理不影响LH分泌（基础分泌或钾诱导的分泌）。使用较高（2.5×10⁻¹⁰ M）或较低剂量的GnRH（1×10⁻¹⁰ M），在有或没有雌二醇致敏（1×10⁻⁹ M）的情况下，检查了ACTH1 - 39（1×10⁻⁸ M或5×10⁻⁷ M；每种组合n = 6个小室）对GnRH诱导的LH分泌的影响。在较低剂量（1×10⁻⁸ M）时，ACTH1 - 39既不影响基础LH分泌，也不影响GnRH诱导的LH分泌。对KCl反应释放的LH也与对照组织和经ACTH处理的组织相似。相反，较高剂量的ACTH1 - 39（5×10⁻⁷ M）在加入培养基后立即增加基础LH分泌（104±3对161±20%），但在2.5×10⁻¹⁰ M GnRH后抑制了GnRH自身预激发效应，即对GnRH 1和GnRH 2的LH反应相似（1786±294对1553±373%）。然而，对照组织和经ACTH处理的组织对KCl的LH反应差异不显著（p > 0.05）（2333±286对2638±431%）。当研究这种较高剂量的ACTH1 - 39对雌二醇预激发的影响时，ACTH增加基础LH分泌，但抑制GnRH的自身预激发效应（1×10⁻¹⁰ M GnRH；945±274对922±323%；p > 0.05），并且与对照相比，对KCl反应释放的LH减少（p < 0.05）（1803±409对4302±1017%）。总之，在体外，ACTH1 - 24既不影响基础LH分泌、GnRH自身预激发效应，也不影响雌二醇敏感性。整个ACTH1 - 39增加基础LH分泌，但降低GnRH自身预激发和雌二醇敏感性。（摘要截断）
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