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The present studies focus on the mechanism of the early action of prostaglandin F2α (PGF2α) on the corpus luteum. In pseudopregnant rats with an intact pituitary, PGF2α produced a significant decrease in accumulation of [l25I]iodo-CG by corpora lutea (-40%; P < 0.01) and plasma progesterone (-56%; P < 0.05) within 2 h. These effects of PGF2α were prevented in animals treated with PRL 6 h before PGF2α injection. Luteal membrane-binding capacity for LH was unchanged within 2 h of PGF2α treatment. Hypophysectomy markedly reduced luteal membrane-binding capacity for LH, accumulation of [125I]iodo-CG by corpora lutea in vivo, and plasma progesterone within 48 h; these effects were prevented by PRL replacement injections. In hypophysectomized control animals, PGF2α did not significantly change [125I]iodo-CG and [125I]iodo-PRL accumulation by corpora lutea in vivo, or plasma progesterone levels. In hypophysectomized PRL-treated animals, PGF2α caused a significant decrease in both [125I]iodo-CG (-69%; P < 0.001) and [125I]iodo-PRL (-38%; P < 0.05) accumulation by corpora lutea as well as a significant decrease in the concentration of plasma progesterone (-60%; P < 0.01). From these studies, it seems that the rapid drop in plasma progesterone levels produced by PGF2α was associated with a decrease in labeled gonadotropin uptake by corpora lutea but not from a loss of gonadotropin receptors.
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Behrman et al. (1978) studied this question.
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