S. Marshall

Serum prolactin levels and prolactin binding activity in adrenals and kidneys of male rats after dehydration, salt loading, and unilateral nephrectomy.

Summary Serum prolactin (PRL) levels and PRL binding activity in microsomal membranes from kidneys and adrenals were measured in control, water-deprived, unilaterally nephrectomized, and salt-loaded male rats. Unilateral nephrectomy and water deprivation increased serum prolactin levels significanty. Unilateral nephrectomy did not alter PRL binding activity in the kidneys, but significantly increased it in the adrenal glands. Salt loading had no effect on serum prolactin levels or PRL binding in the kidneys, but significantly increased PRL binding in the adrenal glands. Inhibition curves and tests of cross reactivity with LH, FSH, TSH, and GH showed that binding of PRL to its receptors in the kidneys and adrenals was specific. These observations suggest that PRL has a role in salt and water metabolism and that PRL receptors in the kidney and adrenals participate in this regulatory system.

Induction of Estrous Cycles in Old Non-Cyclic Rats by Progesterone, ACTH, Ether Stress or L-Dopa

Cycling was induced in old non-cyclic, constant estrous rats by daily injections of progesterone, ACTH or L-dopa or by subjection to ether stress. Progesterone and ACTH were the most effective agents used for re-establishing estrous cycles in these rats. Most of the progesterone- and ACTH-treated rats showed regular cycles, and their ovaries had many corpora lutea; they also showed proestrous serum LH surges. Ether stress and L-dopa mostly induced irregular cycles and fewer corpora lutea in the ovaries; a smaller number of these rats showed proestrous LH surges. After treatment with each of these agents was discontinued, most of the rats returned to constant estrus or irregular cycling.

Effects of estrogen and testosterone on specific prolactin binding in the kidneys and adrenals of rats

Abstract The effects of estradiol benzoate in the female rat, testosterone propionate in the male rat, and castration in both sexes on specific prolactin binding sites in the particulate membranes of the kidneys and adrenals were studied. Castration resulted in a significant increase in PRL binding activity in the kidneys of both males and females, and in a significant increase in PRL binding activity in the adrenals of the females. The increase in PRL binding with castration and the decrease seen with testosterone treatment were similar in both immature and mature rats. Progesterone administration to castrate females failed to alter PRL binding in both tissues. The present results suggest that estrogen and testosterone participate in the PRL osmoregulatory system in the rat.

Prolactin Receptors in Mouse Liver: Species Differences in Response to Estrogenic Stimulation

Summary Serum PRL and hepatic PRL receptors were measured in intact and OVX mice and OVX mice given several doses of EB, OVX significantly increased PRL binding in the liver of female mice, and EB reduced receptors to intact or below intact levels. It was concluded that estrogen decreases PRL receptors in the liver of female mice. This is a striking contrast to the stimulatory effect of estrogen on hepatic PRL receptors in male and female rats. EB elevated serum PRL in OVX mice, but since other investigators reported that PRL does not alter hepatic PRL receptors in female mice, it appears likely that estrogen reduced PRL binding sites by a direct effect on the liver. However, an indirect effect cannot be excluded. In male mice, estrogen increased PRL receptors in the liver as in male rats. The present data demonstrate important species differences between female rats and female mice in estrogenic control of hepatic PRL receptors. Moreover, the inhibitory effect of estrogen in female mice, and its stimulatory action in male mice, suggest that the response of hepatic PRL receptors to estrogen may be sex dependent in different species. The mechanisms of action by which these effects are mediated remain to be clarified.