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雌激素使兔黄体中的甾体生成与3',5'-环磷酸腺苷调节解偶联。

Estrogen uncouples steroidogenesis from 3',5'-cyclic adenosine monophosphate regulation in the rabbit corpus luteum.

作者信息

Townson D H, Keyes P L, Kostyo J L

机构信息

Department of Physiology, University of Michigan Medical School, Ann Arbor 48109-0622, USA.

出版信息

Biol Reprod. 1995 Sep;53(3):718-23. doi: 10.1095/biolreprod53.3.718.

DOI:10.1095/biolreprod53.3.718
PMID:7578698
Abstract

The hypothesis was investigated that estradiol, the luteotrophic hormone in the rabbit, uncouples luteal progesterone production from regulation by LH/cyclic AMP. Progesterone production by corpus luteum (CL) incubated with vehicle, 3-isobutyl-1-methyl-xanthine (IBMX), hCG, or hCG+IBMX was compared in pseudopregnant rabbits treated continuously with estradiol (estradiol-maintained), withdrawn from estradiol for 24-48 h (estradiol-withdrawn), or withdrawn and then replaced with estradiol for 6 or 24 h (estradiol-replaced). Progesterone production in estradiol-maintained rabbits was not altered by hCG and/or IBMX, but was stimulated significantly in estradiol-withdrawn rabbits. This response was reversed (i.e., abolished) in estradiol-replaced (24 h) rabbits. The loss of responsiveness to hCG was not attributable to impaired accumulation of cyclic AMP: basal and hCG-stimulated cyclic AMP concentrations were similar in luteal tissues of estradiol-maintained and estradiol-withdrawn rabbits. The loss of responsiveness to hCG was also not a consequence of maximal progesterone production: CL of estradiol-replaced (6 h) rabbits were also insensitive to hCG, and this occurred before progesterone production attained a maximal rate. We conclude that a striking feature of the luteotrophic action of estrogen is to uncouple the regulation of progesterone production from cyclic AMP.

摘要

研究了如下假说

雌二醇作为兔体内的促黄体生成激素,使黄体孕酮生成与促黄体生成素/环磷酸腺苷(LH/cyclic AMP)的调节解偶联。在持续接受雌二醇处理(雌二醇维持组)、停用雌二醇24 - 48小时(雌二醇撤药组)或撤药后再给予雌二醇6或24小时(雌二醇再给予组)的假孕兔中,比较了用赋形剂、3 - 异丁基 - 1 - 甲基黄嘌呤(IBMX)、人绒毛膜促性腺激素(hCG)或hCG + IBMX孵育的黄体(CL)的孕酮生成情况。在雌二醇维持组兔中,hCG和/或IBMX未改变孕酮生成,但在雌二醇撤药组兔中显著刺激了孕酮生成。在雌二醇再给予(24小时)组兔中,这种反应被逆转(即消失)。对hCG反应性的丧失并非由于环磷酸腺苷积累受损:在雌二醇维持组和雌二醇撤药组兔的黄体组织中,基础和hCG刺激的环磷酸腺苷浓度相似。对hCG反应性的丧失也不是孕酮最大生成量的结果:雌二醇再给予(6小时)组兔的黄体对hCG也不敏感,且这发生在孕酮生成达到最大速率之前。我们得出结论,雌激素促黄体生成作用的一个显著特征是使孕酮生成的调节与环磷酸腺苷解偶联。

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