In Vivo Levels of Prostaglandin F2α, E2 and Prostacyclin in the Corpus Luteum of Pregnant and Pseudopregnant Rats1

Prostaglandin F2α (PGF2α) is a well-known luteolytic factor in the rat corpus luteum. To investigate a possible luteal origin of PGF2α, measurements of this prostaglandin were performed in different luteal tissues in vivo. Prostaglandin E2 (PGE2) and the stable metabolite of prostacyclin, 6-keto-PGF1α, were assayed simultaneously. Corpora lutea of different ages from 57 pregnant and pseudopregnant rats (mated with sterile males) were rapidly excised, dissected in 0°C indomethacin solution, homogenized, and extracted for prostaglandins with solid-phase extraction cartridges. Prostaglandins were determined by radioimmunoassay. Plasma levels of progesterone and 20 α-dihydroprogesterone were also monitored. In the adult pseudopregnant rat model, luteolysis occurs at Day 13 ± 1, and maximal levels of all three prostaglandins were detected on Day 13 of pseudopregnancy: 0.40 ± 0.02, 2.6 ± 0.29, and 1.76 ± 0.24 pmol/mg protein (mean ± SEM, n=7) for PGF2α, PGE2, and 6-keto-PGF1α respectively. In pregnant rats, on the corresponding day, levels were considerably lower: 0.15 ± 0.02, 0.90 ± 0.13, and 0.50 ± 0.06 pmol/mg protein (mean ± SEM, n=9, p < 0.0001), respectively. Luteal levels in pregnant rats showed a continuous decline on Days 13 and 19 for all prostaglandins measured, whereas in pseudopregnant rats an increment of PGF2α was noted between Days 7 and 13 and remained high on Day 19. PGE2 closely followed levels of PGF2α, but at a 5- to 10-fold higher level. The coefficient of correlation between PGF2α and PGE2 in the luteal compartment of both models was 0.87 (p < 0.0001). Prostacyclin content pursued a somewhat different pattern, with peak levels on Days 7 and 13 of pseudopregnancy. In the remainder of the ovary, all prostaglandins measured were fairly constant, and, except for prostacyclin, always lower than in the luteal compartment in both models. It is concluded that luteolysis is accompanied by an increase in luteal availability of PGF2α and that PGF2α of luteal origin, possibly via intercoversion from PGE2, may be the initiating factor in the demise of the corpus luteum.