Acute Effects of Prostaglandin F2αon Ovarian and Luteal Blood Flow, Luteal Gonadotropin Uptakein Vivo,and Gonadotropin Bindingin Vitro*

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Abstract
The mechanism of prostaglandin F2α (PGF2α)-induced luteolysis in mature, day 8 pseudopregnant rats was studied. PGF2α (2.2 mg/kg, sc) treatment resulted in a significant decrease in serum progesterone from 74 ± 4 to 50 ± 4, 44 ± 6, and 44 ± 4 ng/ml (mean ± SE) at 1, 4, and 12 h, respectively. This decrease in luteal function occurred simultaneously with a significant [125I]iodo-CG reduction in uptake by the corpus luteum in situ, but functional blood flow to the corpus luteum was not affected by PGF2α treatment, as assessed by the accumulation of radioactive microspheres (15 μm in diameter). No change in luteal gonadotropin-binding capacity measured in vitro was seen 1 or 4 h after PGF2α treatment, but a significant decrease of 24% in binding capacity occurred 12 h after PGF2α treatment. The affinity constant of the LH receptor remained unchanged (5.6 × 0.1 × 1011 M-1) at all time points studied. A transient but significant increase in functional blood flow to the ovarian interstitial tissue was observed 1 and 4 h after PGF2α treatment, but this increase in interstitial tissue blood flow was not at the expense of the luteal blood supply. The significance of this increase in interstitial blood flow is not known, but the control mechanism may be due to a regional vasodilating effect of PGF2α on follicular tissue. The present studies show that PGF2α-induced inhibition of gonadotropin uptake by the rat corpus luteum in situ was associated with a decrease in serum progesterone, but these effects of PGF2α occurred independently of changes in luteal blood flow or LH receptor content. It is suggested that a block of gonadotropin uptake is an early event in PGF2α-induced luteal regression. Since PGF2α does not block uptake of [125I]-iodo-CG in isolated luteal cells, it is suggested that inhibition of [125I]iodo-CG uptake by PGF2αin vivo is due to restricted access of luteal cells to gonadotropin caused by reduced capillary permeability or impaired interstitial diffusion of gonadotropin.

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