Roles of prostaglandins (PG) F2 alpha, E1, E2, adenosine, oestradiol-17 beta, histone-H2A and progesterone of conceptus, uterine or ovarian origin during early and mid pregnancy in the ewe

Abstract

Pregnancy does not prevent the local transfer or accumulation of prostaglandin F2 alpha (PGF2 alpha) by the corpus luteum (CL), the number of receptors for PGF2 alpha or the binding of PGF2 alpha to the CL. However, the conceptus does depress the response of the CL to PGF2 alpha during early pregnancy. PGE1 and PGE2 appear to be blood-borne antiluteolysins that are delivered locally to prevent the actions of PGF2 alpha during early pregnancy, since they prevent luteolysis only when given by chronic intrauterine infusion adjacent to the ovary with the CL. The concentrations of PGE1 and PGE2 in the endometrium and PGE2 in uterine venous plasma increase during early pregnancy. A Day 10 embryo transferred to a Day 6 progestagen-primed recipient ewe advances the time at which PGE2 is secreted. The uterine venous PGE/PGF2 alpha ratio is 12:1 at midgestation, and exogenous PGF2 alpha increases the placental secretion of oestradiol-17 beta. This is followed by increases in PGE secretion when endogenous PGF2 alpha increases. Both oestradiol-17 beta and PGE may protect placental secretion of progesterone from PGF2 alpha, since PGF2 alpha causes the CL to regress but does not affect placental progesterone or pregnancy in the presence or absence of the ovary.