INDUCTION OF PROLACTIN RECEPTORS BY PROLACTIN IN THE RAT LUNG AND LIVER - DEMONSTRATION OF SEPARATE RECEPTOR AND ANTIBODY ENTITIES

The role of prolactin (PRL) in inducing its own receptors in rat lung and liver beyond the parallel immunological resonse evoked was examined. Ovine PRL (oPRL), mixed with polyvinylpyrrolidone (PVP) and injected s.c. daily to male rats for 7, 10 and 14 days, was shown to induce specific binding of [125I]iodo-oPRL in the lung and liver crude membrane fractions. Doses as low as 12.5 ng/kg were effective in inducing PRL-binding sites, which, however, differed qualitatively from those found in livers of 17b-estrogen-treated male rats. The oPRL-induced sites were highly specific for oPRL and were relatively stable to heat, suggesting the possible participation of antihormone antibodies in the binding observed. Indeed, anti-oPRL antibodies found in sera of oPRL-treated rats increasingly bound oPRL as a function of the duration of treatment. Water-washing of the membrane fraction succeeded in gradually eliminating the loosely bound antibody and in partially restoring the displacing ability of excess (1 .mu.g) rat PRL on oPRL-binding sites in the lung (32.3%) and liver membranes (29.3%). Also restored were the heat lability typical of the receptor site, as well as the inhibitory effect of anti-PRL-receptor antiserum (1:100) on PRL binding (50-65% inhibition of total binding). In keeping with these results, in vitro incubation of liver membranes with rat anti-oPRL antiserum greatly reduced the ability of rat PRL to compete for oPRL binding, supporting the findings after in vivo treatment with oPRL. oPRL injected into male rats is apparently capable of inducing PRL-receptor sites in both lung and liver, in parallel to inducing an immunological response to the heterologous hormone. It is necessary to separate the antibodies accumulating in the membrane fractions in order to study and characterize fully the receptors induced. The demonstrated induction of PRL receptors in the rat lung by PRL itself is in support of the suggested role of PRL in lung surfactant production.