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☆

Abstract

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.