Estrogen uncouples steroidogenesis from 3',5'-cyclic adenosine monophosphate regulation in the rabbit corpus luteum.
Estrogen uncouples steroidogenesis from 3',5'-cyclic adenosine monophosphate regulation in the rabbit corpus luteum.
复制标题
雌激素使兔黄体中的类固醇生成与 3,5-环单磷酸腺苷调节脱钩。
DOI：
10.1095/biolreprod53.3.718
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发表时间：
1995
影响因子：
3.6
通讯作者：
Kostyo,JL
中科院分区：
文献类型：
--
作者：
Townson,DH;Keyes,PL;Kostyo,JL
研究了家兔体内的促黄体激素雌二醇将黄体孕酮的产生与LH/cAMP的调节解偶联的假说。在连续给予雌二醇（雌二醇维持）、停用雌二醇24-48 h（雌二醇停用）或停用后再用雌二醇替代6 h或24 h（雌二醇替代）的假孕兔中，比较了黄体（CL）与溶媒、3-异丁基-1-甲基-黄嘌呤（IBMX）、hCG或hCG+ IBMX孵育后产生的孕激素。孕酮的生产在雌二醇维持兔不改变hCG和/或IBMX，但刺激雌二醇撤回兔显着。在雌二醇替代（24 h）家兔中，该反应逆转（即消除）。对hCG的反应性的丧失并不归因于环AMP的累积受损：雌二醇维持和雌二醇撤回兔的黄体组织中基础和hCG刺激的环AMP浓度相似。对hCG反应性的丧失也不是最大孕酮产生的结果：雌二醇替代（6小时）兔的CL也对hCG不敏感，并且这发生在孕酮产生达到最大速率之前。我们的结论是，一个显着的特点，促黄体作用的雌激素是解耦的调节孕激素的生产周期AMR
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-l-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hCG, or hCG+ IBMX was compared in pseudopregnant rabbits treated continuously with estradiol (estradiol-maintained), withdrawn from estradiol for 24-48 h (estradiol-withdrawn), or withdrawn and then replaced with estradiol for 6 or 24 h (estradiol-replaced).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in estradiol-maintained rabbits was not altered by hCG and/or IBMX, but was stimulated significantly in estradiol-withdrawn rabbits.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 (ie, 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basal and hCG-stimulated cyclic AMP concentrations were similar in luteal tissues of estradiol-maintained and estradiol-withdrawn rabbits.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 AMR