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JOSEPHINE B. MILLER, LANDIS KEY, Progesterone Synthesis in Developing Rabbit Corpora Lutea in the Absence of Follicular Estrogens, Endocrinology, Volume 97, Issue 1, 1 July 1975, Pages 83–90, https://doi.org/10.1210/endo-97-1-83
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We have investigated the role of 17²-estradiol in the early development of therabbit corpus luteum. Ectopic corpora lutea were established in all animals by autotransplanting preovulatory follicles beneath the kidney capsule 6.5 to 8 h after mating (day 0). At this time, the rabbits were bilaterally ovariectomized and in some of these rabbits a Silastic capsule containing crystalline 17²-estradiol was implanted SC. Mean serum concentration of estradiol in rabbits with an estradiol implant was 16.4 pg/ml. In rabbits without an estradiol implant, theestradiol concentration averaged 1 pg/ml despite the presence of transplanted luteinized follicles. Daily blood samples were analyzed for progesterone by radioimmunoassay. Ectopic corporalutea developed in rabbits with or without estradiol treatment. Serum progesterone concentrations inthe two groups increased above castrate values and were not significantly different from one another through day 5.After day 5, progesterone concentrations steadily increased in rabbits treated with estradiol and reached a value of 4.8 ng/ml by day 10. In contrast, serum progesterone steadily decreased after day 5 in rabbits without estradiol treatment to a level of 450 pg/mlby day 10. Hysterectomy on day 0 did not prevent this decline in progesterone, indicating that a uterine luteolytic agent was not involved. Total luteal weight on day 10 was positively correlated with serum progesterone concentration (r = .92; P < 0.01). These results indicate that for a period of approximately 5 days after ovulation, the development of the rabbit ectopic corpus luteum and the secretion of progesterone are autonomous from estradiol secreted by ovarian follicles. After this time, there is an absolute requirement for estrogen which permits further development of the corpus luteum and the continuation of progesterone synthesis. (Endocrinology97: 83,1975)
