Estrogen-Progesterone Antagonism with Respect to Specific Marker Protein Synthesis and Growth by the Uterine Endometrium1

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Abstract
Plasma estrogen does not stimulate peroxidase synthesis by the uterine endometrium in ovulated rats when plasma progesterone [P] levels are high. Administration of exogenous estradiol-17.beta., diethylstilbestrol (DES) or C1628 antagonist transforms these luteal phase cells into follicular phase cells capable of synthesizing peroxidase in the presence of P. Studies with immature and spayed rats indicate that the P block to peroxidase synthesis can be released through administration of exogenous estrogen, DES or C1628. Data indicate that in the presence of estrogen (or antagonist) and P, the estrogenic effect is expressed through synthesis of specific proteins (peroxidase), but P blocks the growth-promoting effects of estrogen. P antagonism to estrogen action does not result from blocks to: entry of estrogen into target cells, estrogen binding to the receptor, the temperature-dependent transformation of native (4S) to the active (5S) complex and entry into and binding of the active complex to chromatin in target cells. P effects reduction in cytoplasmic estrogen receptor levels especially when administered along with estrogen. Such reductions in receptor are believed to at least partially explain the P antagonism.