Luteolysis induced by a prostaglandin F2α analogue occurs independently of prolactin in the rat

The hypothesis that prolactin exerts a stimulatory dominance over the luteolytic effect of prostaglandin (FG) F-2 alpha on corpus luteum maintenance and progesterone production was experimentally tested. A dose-dependent effect of the stable PGF2 alpha analogue cloprostenol (dose range 200 ng-5 (mu g) 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 20 alpha-dihydroprogesterone significantly (p < 0.05) increased (by 80%) initially at a 0,5-mu g dose of cloprostenol. To study the integrated response to prolactin and PCF2 alpha, 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 mu g cloprostenol the LN receptor mRNA levels and the serum progesterone/20 alpha-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 PGF(2 alpha).