Effect of PGF(2α), indomethacin, tamoxifen, or estradiol-17β on incidence of abortion, progesterone, and pregnancy-specific protein B (PSPB) secretion in 88- to 90-day pregnant sheep

One objective of this experiment was to evaluate our hypotheses that estradiol-17β regulates secretion of pregnancy specific protein B (PSPB) and that secretion of progesterone during pregnancy is regulated by a prostanoid by examining the effects of prostaglandin F(2α) (PGF(2α)), a luteolyic agent; indomethacin, a prostanoid synthesis inhibitor; tamoxifen, an estrogen receptor antagonist; estradiol 17-β; and interaction of these factors on the incidence of abortion and progesterone and PSPB secretion. Another objective was to determine if there is a luteal source of PSPB. Weights of corpora lutea were decreased (P ≤ 0.05) by PGF(2α), indomethacin, PGF(2α) + tamoxifen, PGF(2α) + indomethacin, and PGF(2α) + estradiol-17β but not (P ≥ 0.05) by tamoxifen or estradiol-17β alone. No ewe treated with PGF(2α) alone aborted (P ≥ 0.05). Forty percent of ewes treated with PGF(2α) + estradiol-17β aborted (P ≤ 0.05), but ewes were not aborted by any other treatment within the 72-h sampling period. Profiles of progesterone in jugular venous blood differed (P ≤ 0.05) among control, indomethacin-, tamoxifen-, and PGF(2α) + indomethacin-treated ewes. Progesterone in jugular venous blood of control ewes decreased (P ≤ 0.05) by 24 h, followed by a quadratic increase (P ≤ 0.05) from 24 to 62 h. Progesterone in jugular venous blood of indomethacin-, PGF(2α)-, PGF(2α) + tamoxifen-, PGF(2α) + indomethacin-, PGF(2α) + estradiol-17β-, and tamoxifen-treated ewes was reduced (P ≤ 0.05) by 18 h and did not vary (P ≥ 0.05) for the remainder of the 72-h sampling period. Progesterone in vena cava and in uterine venous blood was reduced (P ≤ 0.05) at 72 h in PGF(2α)-, indomethacin-, tamoxifen- , PGF(2α) + indomethacin-, PGF(2α) + tamoxifen-, and PGF(2α) + estradiol- 17β-treated ewes. Weights of placentomes did not differ among treatment groups (P ≥ 0.05). Profiles of PSPB in inferior vena cava blood differed (P ≤ 0.05) among control, estradiol-17β-, indomethacin-, tamoxifen-, PGF(2α) + indomethacin-, and PGF(2α) + tamoxifen-treated 88- to 90-day pregnant ewes. Concentrations of PSPB in inferior vena cava blood were increased (P ≤ 0.05) in indomethacin-, estradiol-17β-, tamoxifen-, PGF(2α) + tamoxifen-, and PGF(2α) + indomethacin-treated 88- to 90-day pregnant ewes within 6 h and did not vary (P ≥ 0.05) for the remainder of the 72-h sampling period. Concentrations of PSPB in uterine venous blood of indomethacin-, tamoxifen-, PGF(2α) + tamoxifen-, and PGF(2α) + indomethacin-treated ewes were greater (P ≤ 0.05) at 72 h than at 0 h. PSPB in ovarian venous blood did not differ (P ≥ 0.05) adjacent or opposite to the ovary with the corpus luteum. It is concluded from these data that estrogen regulates placental secretion of PSPB and that a prostanoid, presumably prostaglandin E, regulates placental secretion of progesterone during 88-90 days of gestation in sheep and that there is no luteal source of PSPB.