The exact mechanisms controlling uterine secretion of prostaglandin F2α (PGF2α) are not known. This study (Experiments 1, 2 and 3) was conducted to evaluate the relationships of progesterone and estrogen to changes in 13,14-dihydro-1S-keto-prostaglandin F2α (PGFM) and PGF2α in ewes. Experiment 1 was designed to determine whether a radioimmunoassay (RIA) for progesterone would detect pessary-released 6α-methyl-17α-hydroxy-progesterone (MPA; n=3) and oral 17α-acetoxy-6-methyl-16-methylene-4, 6-pregnadiene-3, 20 dione (MGA; n=3) in blood plasma of ovariectomized ewes. Neither progestogen treatment interfered with the RIA. Experiment 2 was conducted to answer the question: Do MPA-containing pessaries delay luteolysis in intact ewes? Ewes were treated with MPA containing (n=10) or blank pessaries (controls; n=8) from d 7 and until d 18 of the estrous cycle for control and until d 22 for MPA-treated ewes; d 0 was the day of estrus. Blood samples were collected from the jugular vein throughout the experiment. Pessaries containing MPA did not affect the timing of luteolysis (d 15.4 ± .2), but they prolonged (P<.O5) the interestrous interval (17.5 d for control vs 24.1 d for MPA-treated ewes). Experiment 3 was designed to study the relationships among progesterone, estrogen, PGFM and PGF2α in ewes. Ewes were treated with MPA-containing (n=7; 60 mg), progesterone-containing (n=8i 45 mg) or blank pessaries (n=8) from d 7 until d 20 of the estrous cycle. From d 14 and continuing until 24 h after estrus, jugular and vena caval blood samples were collected during two sampling periods daily. Plasma was assayed for progesterone, estrogen, PGFM and PGF2α. Treatment did not affect the profiles of change in concentration of progesterone, PGFM and jugular PGF2α, but treatment affected (P < .05) estrogen and vena caval PGF2α profiles. Overall, treatment affected (P < .05) the mean concentrations of estrogen, progesterone, PGFM and PGF2α. sampling site (jugular vs. vena cava) affected (P < .0001) the mean concentration of progesterone, estrogen and PGF2α, but site did not affect PGFM concentrations. Hormonal relationships associated with changes in release of PGF2α were evaluated. Estrogen seemed to be the primary hormone controlling PGF2α release. In conclusion, MPA treatment did not delay the timing of luteolysis, but it increased the interestrous interval. Of the compounds measured, estrogen accounted for the greatest proportion of the variation in PGF2α release in ewes around the time of luteolysis.
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