Increased LH receptor mRNA and extended corpus luteum function induced by prolactin and indomethacin treatment in vivo in hysterectomized pseudopregnant rats.

To assess the effects of prostaglandins and prolactin on corpus luteum function and regression, sterile-mated adult pseudopregnant rats hysterectomized on day 5 after mating were injected with indomethacin or prolactin. Daily samples of blood were collected via the tail, from day 12 to day 21, and assayed for serum concentrations of progesterone, 20 alpha-dihydroprogesterone and LH, whereafter corpora lutea and the remainder of ovaries were separated and the tissue content of PGF2 alpha, PGE2 and LH receptor mRNA were measured. Injections of prolactin (8 iu) s.c. or a low dose of indomethacin (200 micrograms kg-1) s.c. were administered twice a day, beginning on day 13 after mating. Both indomethacin and prolactin significantly increased serum progesterone concentrations (P < 0.05; n = 8), and extended the period of functional corpora lutea when compared with controls. Indomethacin, but not prolactin, lowered the concentration of serum 20 alpha-dihydroprogesterone. In the corpora lutea of indomethacin-treated animals, collected on day 21, both prostaglandins measured were reduced in concentration by 50% or more, compared with controls (P < 0.05; n = 8), whereas prolactin had no effect. Both prolactin and indomethacin treatment caused a substantial (tenfold) increase in the concentration of LH receptor mRNA, confined solely to the luteal compartment. These findings in vivo provide further evidence for a luteolytic role of locally synthesized prostaglandins in the rat ovary. Furthermore, prolactin can sustain corpus luteum function by exerting a luteotrophic effect during the late luteal phase, as judged by the stimulation of progesterone synthesis and the expression of LH receptors.