On the possible role of the liver in the galactopoietic action of prolactin in the rat

Abstract

The possibility that the liver contributes to the galactopoietic effects of PRL was assessed in lactating rats in which endogenous PRL secretion was suppressed by injections of bromocriptine. Pup weight gain over a 5-day period (i.e. days 7-12 of lactation) was used as an index of lactational performance in dams. Osmotic minipumps were used to infuse different doses of ovine (o) PRL into either the external jugular vein (JV) or the hepatic portal vein of the dams at a constant rate. The latter route of delivery would directly expose the liver to a higher concentration of PRL than would the former one. Twice daily sc injections of bromocriptine (1.5 mg/kg.injection) in corn oil into the dams completely suppressed litter weight gain. Infusion of oPRL into the JV at a dose of 2.0 mg/rat.day restored lactation to normal in the drug-treated mothers. Electrophoretic analysis indicated that about 95% of the oPRL remained in the intact monomeric form when incubated in the infusion solvent in the minipump at 37 C for 2 days, but by 4 and 6 days of incubation the amounts of that form decreased by about 25% and 50%, respectively. Measurement of serum oPRL levels by RIA showed that they were fairly constant, and after 5 days of infusion, the final concentration was directly related to the dose infused. Continuous infusion of oPRL into the JV was equally effective at restoring pup weight gain as was infusion into the hepatic portal vein over a wide range of doses. Hence, a physiological role of the liver in the maintenance of lactation by PRL is not supported by these experiments.