Effects of prostaglandin E and F receptor agonists in vivo on luteal function in ewes

Loss of progesterone secretion at the end of the estrous cycle is via uterine PGF2α secretion; however, uterine PGF2α is not decreased during early pregnancy in ewes to prevent luteolysis. Instead the embryo imparts resistance to PGF2α-induced luteolysis, which is via the 2-fold increase in prostaglandins E1 and E2 (PGE1, PGE2; PGE) in the endometrium during early pregnancy. Chronic intrauterine infusion of PGE1 or PGE2 prevents spontaneous or an estradiol-17β, IUD, or PGF2α-induced luteolysis. Four PGE receptor subtypes (EP1, EP2, EP3, and EP4) and an FP receptor specific for PGF2α have been identified. The objective of this experiment was to determine the effects of EP1, EP2, EP3, or FP receptor agonists in vivo on luteal mRNA for LH receptors, occupied and unoccupied LH receptors, and circulating progesterone in ewes. Ewes received a single treatment of 17-phenyl-tri-Nor-PGE2 (EP1, EP3), butaprost (EP2), 19-(R)-OH-PGE2 (EP2), sulprostone (EP1, EP3), or PGF2α (FP) receptor agonists into the interstitial tissue of the ovarian vascular pedicle adjacent to the luteal-containing ovary. 17-Phenlyl-tri-Nor-PGE2 had no effect (P ≥ 0.05) on any parameter analyzed. Butaprost and 19-(R)-OH-PGE2 increased (P ≤ 0.05) mRNA for LH receptors, occupied and unoccupied LH receptors, and circulating progesterone. Both sulprostone and PGF2α decreased (P ≤ 0.05) mRNA for LH receptors, occupied and unoccupied LH receptors, and circulating progesterone. It is concluded that both EP3 and FP receptors may be involved in luteolysis. In addition, EP2 receptors may mediate prevention of luteolysis via regulation of luteal mRNA for LH receptors to prevent loss of occupied and unoccupied LH receptors and therefore to sustaining luteal function.