Luteolysis Induced by a Prostaglandin F₂ Analogue Occurs Independently of Prolactin in the Rat¹

^a Department of Physiology, Umeå University, S-90187 Umeå, Sweden ^b Department of Obstetrics and Gynecology, Umeå University Hospital, S-90185, Umeå, Sweden

The hypothesis that prolactin exerts a stimulatory dominance over the luteolytic effect of prostaglandin (PG) F₂ on corpus luteum maintenance and progesterone production was experimentally tested.

A dose-dependent effect of the stable PGF₂ analogue cloprostenol (dose range 200 ng<<014>>5 µg) 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-dihydroprogesterone significantly (p < 0.05) increased (by 80%) initially at a 0.5-µg dose of cloprostenol.

To study the integrated response to prolactin and PGF₂, 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 µg cloprostenol the LH receptor mRNA levels and the serum progesterone/20-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 PGF₂.

¹ The present study was supported by the Medical Research Council of Sweden (11556, 11832, and 12604), Novo Nordisk foundation, The Swedish Society of Medicine, and The Swedish Society for Medical Research.

² Correspondence: Erik Bjurulf, Department of Obstetrics and Gynecology, Umeå University Hospital, S-90185, Umeå, Sweden. FAX: 46-90- 7866683; erik.bjurulf{at}physiol.umu.se

³ Reprint requests: Jan Olofsson, Department of Obstetrics and Gynecology, Umeå University Hospital, S-90185, Umeå, Sweden. FAX: 46-90- 773905; jan.olofsson{at}obstgyn.umu.se

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