It is possible that creation of lower than normal luteal phase concentrations of progesterone or progestogen treatment could have direct effects on the ovary. Certainly, the CL can exert local effects on developing follicles in sheep in spite of morphological barriers between the luteal and follicular compartments, and the high concentrations of progesterone in ovine follicular fluid (10-fold to 40-fold serum concentrations; ). Progesterone may modify follicular responsiveness to gonadotropins in both CL-bearing and non-CL-bearing ovaries. It is also feasible that circulating concentrations of progesterone or MAP could affect ovarian follicles indirectly by extrao-varian mechanisms. Luteal progesterone may alter the countercurrent transfer of hormones in the subovarian vascular plexus, probably via changes in estrogen:progesterone ratios and their effects on the constriction of blood vessels.
In the ewes of the present study, even though MAP sponges were inserted on the day of PGF2a treatment, injection of a luteolytic dose of PGF2a on —Day 8 after ovulation was followed by ovulation of some large follicles, between Days 1 and 6 after injection. There was no change in circulating concentrations of FSH in samples taken daily during that period, but a rapid decline in daily serum concentrations of estradiol to basal concentrations in the six ovulating ewes after PGF2a/MAP treatment coincided with the day of ovulation (experiment 1). Such a decline in serum concentrations of estradiol is typically seen around ovulation during the normal estrous cycle. We initially suspected that PGF2a-induced luteolysis in the presence of MAP resulted in aberrant or truncated preovulatory changes in gonadotropin release. Obviously, in cyclic ewes, there is tremendous variation in the magnitude and duration of the preovulatory LH surge. However, frequent blood sampling conducted on Day 3 after PGF2a did not indicate the occurrence of phasic secretion of LH in the treated ewes. Moreover, based on blood sampling every 4 h throughout the period of treatment with MAP (experiment 2), there was no evidence of a preovulatory mode of gonadotropin secretion.