Estrogen-Induced Progesterone Receptor in the Syrian Hamster Kidney. IL Modulation by Synthetic Progestins*

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Abstract
The estrogen-induced progesterone receptor in the untransformed hamster kidney has been further characterized. The ability of various estrogenic hormones to induce specific renal progesterone receptor in the hamster was 17β-estradiol = estrone > estriol > 17α-estradiol. At the period of maximum progesterone receptor induction by either diethylstilbestrol (DES) or 17β-estradiol, hormone withdrawal resulted in a linear decline in progesterone receptor content to nearly castrate levels after 5 weeks. Readministration of estrogen in these hormonewithdrawn animals elicited a significant increase in progesterone receptor concentration in the kidney compared to castrate levels after only 9 days of treatment. In contrast to this anamnestic progesterone receptor response, a significant elevation in progesterone receptor concentration does not occur in previously untreated DES-primed hamsters until 19–24 days of treatment. Since progesterone had no appreciable affect on the ability of estrogen to induce progesterone receptor and androgen in combination with DES completely suppressed the induction of progesterone receptor, the effects of various androgenic progestins were examined for their ability to affect progesterone receptor induction by estrogen. The presence of either medroxyprogesterone acetate or megestrol acetate reduced the amount of progesterone receptor by nearly 50% compared to levels in animals treated with DES alone. In comparison, medroxyprogesterone was virtually ineffective in preventing progesterone receptor induction when used in combination with estrogen. Both nortestosterone and norethindrone were nearly as effective as 5α-dihydrotestosterone in depressing progesterone receptor induction as a result of DES treatment. These results are consistent with the ability of these androgenic progestins to compete for the 9S cytosolic androgen receptor in the hamster kidney; that is, 5α-dihydrotestosterone > norethindrone ≥ nortestosterone > megestrol acetate ≥ medroxyprogesterone acetate > medroxyprogesterone > progesterone. These observations indicate that the effects of androgenic progestins on progesterone receptor induction by estrogen are mediated via the androgen receptor. (Endocrinology108: 1751, 1981)

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