Effect of PCF2α, 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-17 beta 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-2 alpha (PGF(2 alpha)), a luteolyic agent; indomethacin, a prostanoid synthesis inhibitor; tamoxifen, an estrogen receptor antagonist; estradiol 17-beta; 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 less than or equal to 0.05) by PGF(2 alpha), indomethacin, PGF(2 alpha) + tamoxifen, PGF(2 alpha) + indomethacin, and PGF(2 alpha) + estradiol-17 beta but not (P greater than or equal to 0.05) by tamoxifen or estradiol-17 beta alone. No ewe treated with PGF(2 alpha) alone aborted (P greater than or equal to 0.05). Forty percent of ewes treated with PGF(2 alpha) + estradiol-17 beta aborted (P less than or equal to 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(2 alpha) + indomethacin-treated ewes. Progesterone in jugular venous blood of control ewes decreased (P less than or equal to 0.05) by 24 h, followed by a quadratic increase (P less than or equal to 0.05) from 24 to 62 h. Progesterone in jugular venous blood of indomethacin-, PGF(2 alpha)-, PGF(2 alpha) + tamoxifen-, PGF(2 alpha) + indomethacin-, PGF(2 alpha) + estradiol-17 beta-, and tamoxifen-treated ewes was reduced (P less than or equal to 0.05) by 18 h and did not vary (P greater than or equal to 0.05) for the remainder of the 72-h sampling period. Progesterone in vena cava and in uterine venous blood was reduced (P less than or equal to 0.05) at 72 h in PGF(2 alpha)-, indomethacin-, tamoxifen-, PGF(2 alpha) + indomethacin-, PGF(2 alpha) + tamoxifen-, and PGF(2 alpha) + estradiol-17 beta-treated awes. Weights of placentomes did not differ among treatment groups (P greater than or equal to 0.05). Profiles of PSPB in inferior vena cava blood differed (P less than or equal to 0.05) among control, estradiol-17 beta-, indomethacin-, tamoxifen-, PGF(2 alpha) + indomethacin-, and PGF(2 alpha) + tamoxifen-treated 88- to 90-day pregnant ewes. Concentrations of PSPB in inferior vena cava blood were increased (P less than or equal to 0.05) in indomethacin-, estradiol-17 beta-, tamoxifen-, PGF(2 alpha) + tamoxifen-, and PGF(2 alpha) + indomethacin-treated 88- to 90-day pregnant ewes within 6 h and did not vary (P greater than or equal to 0.05) for the remainder of the 72-h sampling period. Concentrations of PSPB in uterine venous blood of indomethacin-, tamoxifen-, PGF(2 alpha) + tamoxifen-, and PGF(2 alpha) + indomethacin-treated ewes were greater (P less than or equal to 0.05) at 72 h than at 0 h. PSPB in ovarian venous blood did not differ (P greater than or equal to 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. (C) 1999 Elsevier Science Inc. All rights reserved.