Kirchick H J, Birnbaumer L
Endocrinology. 1981 Dec;109(6):2129-37. doi: 10.1210/endo-109-6-2129.
We have reported in recent studies that exogenous estradiol (E2) suppresses luteal LH-responsive adenylyl cyclase activity in pseudopregnant rabbits. The purpose of the present study was to determine whether this suppression is reversible. High or low level E2-filled Silastic capsules or empty capsules were sc implanted in day 5 pseudopregnant rabbits. On day 8 of pseudopregnancy, the high level E2 implants were either sham replaced, replaced with low level E2 implants, or replaced with empty capsules. The low level E2 implants and empty capsules were sham replaced. Animals from each of the five resulting groups were killed on days 9-12 of pseudopregnancy (1, 2, 3, and 4 days postimplant manipulation). As previously reported using an intermittent injection protocol, exogenous E2 had little effect upon serum progesterone concentrations. Both high and low level E2 implants suppressed the luteal LH-responsive adenylyl cyclase, but the suppression due to the low level E2 implants was not as great as that for the high level E2 implants. Within 24 h of switching from high to low level E2 implants, LH-responsive adenylyl cyclase activity increased from the level found for animals with high level E2 throughout to that found for animals with low level E2 throughout. Total withdrawal of exogenous E2 resulted in a precipitous fall in serum progesterone concentrations, as predicted by previous studies. However, within 4 days of withdrawal, both serum progesterone and luteal LH-responsive adenylyl cyclase activity had returned to control values. E2 implants also suppressed serum LH concentrations and follicular LH-responsive adenylyl cyclase activities. Both of these effects were reversed within 24-48 h after implant withdrawal. We conclude, therefore, that effects of exogenous E2 are reversible and that the previously reported E2-induced dependency upon exogenous E2 is related to the experimental protocol used.
我们在最近的研究中报道，外源性雌二醇（E2）可抑制假孕兔黄体中促黄体生成素（LH）反应性腺苷酸环化酶的活性。本研究的目的是确定这种抑制是否可逆。将高剂量或低剂量E2填充的硅橡胶胶囊或空胶囊皮下植入第5天的假孕兔体内。在假孕第8天，将高剂量E2植入物进行假更换，换成低剂量E2植入物，或换成空胶囊。低剂量E2植入物和空胶囊进行假更换。在假孕的第9 - 12天（植入物操作后1、2、3和4天）处死来自五个结果组中的每一组动物。如先前使用间歇性注射方案所报道的，外源性E2对血清孕酮浓度影响很小。高剂量和低剂量E2植入物均抑制黄体中LH反应性腺苷酸环化酶，但低剂量E2植入物引起的抑制不如高剂量E2植入物那么大。从高剂量E2植入物切换到低剂量E2植入物后的24小时内，LH反应性腺苷酸环化酶活性从整个过程中高剂量E2动物的水平增加到整个过程中低剂量E2动物的水平。如先前研究所预测的，外源性E2的完全撤除导致血清孕酮浓度急剧下降。然而，在撤除后的4天内，血清孕酮和黄体中LH反应性腺苷酸环化酶活性均恢复到对照值。E2植入物还抑制血清LH浓度和卵泡中LH反应性腺苷酸环化酶活性。这两种作用在植入物撤除后24 - 48小时内均被逆转。因此，我们得出结论，外源性E2的作用是可逆的，并且先前报道的E2诱导的对外源性E2的依赖性与所使用的实验方案有关。
