The hypothesis that 17β-estradiol suppresses dopamine secretion into hypophysial portal blood was tested. Portal plasma concentrations of dopamine were significantly lower in proestrous rats (1.0 ± 0.1 ng/ml; mean ± SE) than in estrous rats (1.9 ± 0.38 ng/ml). To deplete the animal of endogenous steroid hormones, proestrous rats were adrenalectomized (Adx) and ovariectomized (Ovx). Twenty-four hours later, hypophysial portal blood was collected for 60 min, and the plasma from this blood was analyzed for dopamine. Arterial plasma from these rats was assayed for 17β-estradiol and progesterone. The concentrations of dopamine in the portal plasma of sham-operated rats and bilaterally Adx-Ovx rats were similar to those in estrous animals. The concentration of dopamine in portal plasma of Adx-Ovx rats injected 24 h earlier with 50 μg 17β-estradiol was 1.0 ± 0.31 ng/ml, which was comparabExposure of adipocytes from young rats (2–3 months old) to dexamethasone in vitro results in 40–50% inhibition of glucose transport and metabolism. ComparabThe effects of progesterone, testosterone, corticosterone, and TRH on estrogen-induced PRL synthesis andcytoplasmic estrogen receptor levels were studied in a clonalstrain of rat pituitary tumor cells (GH3). PRL synthesis wasmeasured as the amount of hormone which accumulated in theculture medium (micrograms per mg cell protein/24 h), andreceptor levels were measured as specific [3H]estradiol bindingin the GH3 cells (picomoles per mg cell protein). 17β-Estradiol (10-8M) stimulated PRL synthesis 2.1-fold, while progesterone (10-6 M) and corticosterone (10-6 M) bothdecreased PRL synthesis to about 0.9 times control levels. Testosterone(10-6 M) and TRH (3 × 10-7 M) increased PRL synthesis1.2- and 1.8-fold, respectively. The combined treatmentwith 17β-estradiol plus progesterone increased PRL synthesis1.2-fold, while the simultaneous treatment with either 17β8-estradiol and corticosterone or 17β-estradiol and testosterone stimulated PRL synthesis to values not significantly different from those in cultures treated with 17/8-estradiol alone. In contrast, the stimulatory effects of 17β-estradiol and TRH were additive. The antagonistic effects of progesterone on estrogen-induced PRL synthesis were not due to competition with 17β-estradiol for binding to the estrogen receptor. Treatment with progesterone, but not with the other hormones, reduced estrogen receptor levels in the GH3 cells, but did not change the binding affinity between [3H]estradiol and its receptor. The inhibitory effect of progesterone was significant (P < 0.03) at 10-10 M and maximal at 10-6 M, decreasing specific [3H]estradiol binding from 0.283 ± 0.007 in control cultures to 0.055 ± 0.006 (mean ± SE) pmol/mg cell protein. The progesterone effect was detectable after 2 days and maximal after 4 days of treatment. These data suggest strongly that progesterone inhibits estrogen- induced PRL synthesis by decreasing the number of available receptor sites. © 1979 by The Endocrine Society.
