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Luteolysis induced by a prostaglandin F2alpha analogue occurs independently of prolactin in the rat.

The hypothesis that prolactin exerts a stimulatory dominance over the luteolytic effect of prostaglandin (PG) F2alpha on corpus luteum maintenance and progesterone production was experimentally tested. A dose-dependent effect of the stable PGF2alpha analogue cloprostenol (dose range 200 ng(-5) microg) was found 12 h after s.c. injection, in Day 9 adult pseudopregnant rats: 1) LH receptor mRNA levels, as measured by RNase protection assay, were dramatically decreased (by 67%) by a single s.c. dose of 200 ng cloprostenol; and 2) serum progesterone levels were significantly (p < 0.05) decreased (by 43%) whereas 20alpha-dihydroprogesterone significantly (p < 0.05) increased (by 80%) initially at a 0.5-microg dose of cloprostenol. To study the integrated response to prolactin and PGF2alpha, we investigated the effect of cloprostenol treatment in sterile-mated female rats with or without circulating prolactin. Prolactin secretion was inhibited by s.c. injection of bromocriptine (1 mg) in the morning of the ninth day of pseudopregnancy. A group of rats was left prolactin-depleted; in another group prolactin was reintroduced by adding 8 IU ovine prolactin. It was found that after injection of 0.5 microg cloprostenol the LH receptor mRNA levels and the serum progesterone/20alpha-dihydroprogesterone ratio were not significantly different whether the rats had circulating endogenous/exogenous prolactin or were prolactin-depleted. Therefore, although prolactin exerts a stimulatory influence on both progesterone production and corpus luteum LH receptor gene expression, the conclusion is reached that prolactin alone cannot antagonize the luteolytic effect of PGF2alpha.