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PubMed1976

Induction of lactogenic receptors. II. Studies on the liver of hypophysectomized male rats and on rats bearing a growth hormone secreting tumor.

The role of growth hormone (GH), as well as prolactin and ACTH, in the induction of the PRL receptor was investigated both in hypophysectomized male rat livers and in the livers of male rats bearing a GH secreting tumor. After 7 days of s.c. injections, specific binding (% SB) of PRL in controls and rats treated with oPRL, hGH, ACTH, hCG, estradiol (E2), or testosterone (T) was approximately 1%. Treatment with oPRL plus ACTH increased SB to 4%; adding E2 to this combination produced a further increase to 8%, whereas the addition of T decreased hepatic binding to 1%. Combination of hGH with ACTH was most effective, giving a SB of 33%, which is similar to that observed in the liver of rats bearing a GH secreting tumor (36%). These studies suggest that GH acts synergistically with PRL and/or ACTH to increase lactogenic binding sites in the male rat liver and that sex steroids have a modulating effect on this action.

Adrenocorticotropic Hormone↗
PubMed1976

Effect of a synthetic corticoid on milk yield and composition and on blood metabolites and hormones in dairy cows.

Twenty-five dairy cows were assigned randomly by breed to flumethasone treatment (10 mug/day, 13 cows) or placebo control (12 cows) from 4 to 44 wk of lactation. Lactation means and trends with stage of lactation were treatment responses. Mean milk yields of cows supplemented with flumethasone were not significantly different from controls. Mean metabolite (glucose, nonesterified fatty acids, and total esterified fatty acids) and hormone concentrations (corticoids, insulin, and prolactin) of blood plasma and their trends throughout lactation were unaffected by supplementation. Data were pooled to determine effects of stage of lactation, temperature, pregnancy, and month on these variables. Changes during lactation were systematic for feed intake, body weight, milk yield, milk components except somatic cells, blood metabolites, and prolactin. At environmental temperatures above 18 C, effects were consistently negative for milk yield and composition, but only above 26 C for feed intake. Prolactin of plasma increased with increasing temperature to 18.2 C and then decreased. No other plasma metabolite or hormone was affected by days pregnant, age, or temperature. Months affected feed intake, milk yield, milk fat percentages, all blood metabolites, and prolactin. Prolactin concentrations increased as daylight hours increased. Our inability to augment established lactation by feeding a supplement of synthetic glucocorticoid to lactating cows is consistent with the view that a lack of avialable corticoids does not limit persistency of lactation in the cow.

Animals↗
PubMed1976

Failure to demonstrate transfer of milk prolactin into blood of milk-fed rats and calves.

Possible absorption of ingested prolactin into blood of milk-fed neonates was studied in two species by different experimental approaches. In calves, secretion of endogenous prolactin was suppressed by administration of ergocryptine. Prolactin was measured in blood plasma at 20-min intervals before and after ingestion by the calves of bovine milk or colostrum which contained prolactin. Prolactin in plasma during the 2-h period after feeding was the same as that during the 1-h period before feeding. therefore, these data failed to demonstrate any absorption of ingested prolactin into the blood of neonatal calves. Previous research showed that bovine prolactin could be transferred into rat milk by injecting it into lactating rats. Blood serum was collected from rat pups that were suckling dams previously injected with bovine prolactin. Several dosages and times of administration were used in the experimental design, and blood serum also was collected from rat pups nursing control dams. All samples were immunoassayed for bovine prolactin with reagents that crossreacted only slightly with endogenous rat prolactin. Injection of lactating dams with bovine prolactin did not increase the amount of immunoreactive bovine prolactin in the sera of suckling rat pups. These results agree with those from the calf study and indicate that ingested bovine prolactin was not absorbed intact into the blood of neonatal rats.

Absorption↗
PubMed1975

[Ultrastructure of the prolactin cells of the pituitary gland of female rats after stimulation with norethisterone enanthate].

Prolactine cells of rat anterior pituitary gland were studied with the electron microscope in thin sections and freeze-etch replicas after treatment with norethisterone-oenanthate. A pathological secretory process is caused in this cell type in rats, when treated with this compound. Prolactine cells grow in number and volume of single cells. This is especially due to an enormous proliferation of the Golgi apparatus. In the same time, however, exocytosis of hormonal secretory granules is apparently reduced. Therefore, serum hormone level remains nearly normal.

Animals↗
PubMed1977

Prolactin binding in ovariectomy-responsive and ovariectomy-nonresponsive rat mammary carcinoma.

Growth of the transplantable mammary tumor, MTW9, in W/Fu rats is greatly enhanced by elevated serum prolactin concentrations. This report compares the prolactin binding to tumor membranes in two mammary tumor strains derived from MTW9. Maximum binding to membranes of both tumors occurred at pH 7.6 after incubation for 30 hr at 4 degrees. The binding was inhibited only by polypeptide hormones that possess lactogenic activity. MTW9-P, an ovariectomy-responsive tumor developed in rats maintained on daily perphenazine injections, had 4-fold-higher prolactin binding than had MTW9MtT, an ovariectomy-nonresponsive tumor developed in rats bearing the mammosomatotropic pituitary tumor, MtTW10. Withdrawal of perphenazine from rats bearing MTW9-P caused a fall to normal of plasma prolactin, no tumor regression, and no significant change in prolactin binding. In contrast, resection of MtT resulted in tumor regression, a fall to normal of serum prolactin, and a nearly 3-fold increase in prolactin binding. Scatchard plots of prolactin binding data yield an apparent affinity constant, Ka, of 1.2 X 109 liters/mole for both tumors. The 4-fold-higher prolactin binding in the ovariectomy responsive variant suggests a positive correlation between ovariectomy response and the number of membrane prolactin-binding sites. No correlation between prolactin sensitivity and prolacting binding is apparent.

Animals↗
PubMed1977

Prolactin binding to R3230AC mammary carcinoma and liver in hormone-treated and diabetic rats.

Specific 125I-labeled prolactin binding was measured in membrane particles prepared from R3230AC mammary carcinoma and liver of tumor-bearing Fischer rats after either prolactin, estrogen, or lergotrile mesylate treatment, or after the induction of diabetes by streptozotocin. Hormone binding to tumors was decreased by treatment with prolactin (0.5 or 1 mg/day) or estradiol valerate (7.5 mg/kg/week). In contrast, prolactin treatment did not affect prolactin binding to liver membrane particles, but estradiol valerate treatment resulted in a four-fold increase in prolactin binding to this tissue. Lergotrile mesylate, which lowers plasma prolactin levels, did not affect tumor growth or prolactin binding to either tumor or liver. Prolactin binding to both tumor and liver was significantly reduced in diabetic rats, suggesting that insulin may play an important role in controlling tissue sensitivity to prolactin. Specific binding of 125I-labeled prolactin to enzymatically dissociated cells from R3230AC tumors was demonstrated in vitro. The binding capacity of the cells was found to be of the same order of magnitude as the binding capacity in membrane preparations when appropriate corrections were applied for yields of cells and membranes. R3230AC tumor, which is responsive to prolactin appears therefore to be a useful model system for further study aimed at elucidation of growth and metabolic response to the hormone prolactin in breast cancer.

Acetonitriles↗
PubMed1977

[Antigonadotropic actions of prolactin. Study of 10 cases of women with hyperprolactinemia].

In order to determine the pituitary or ovarian site of the anti-gonadotrophic action of prolactin (PRL), ten women with hyperprolactinaemia were studied in the following way: 1) Repeated estimations of PRL, gonadotrophins (LH and FSH), plasma estradiol and progesterone during six weeks of treatment with bromocriptine. 2) Verification of the effects of estradiol benzoate on LH and FSH levels before and after normalisation of prolactin. 3) Exploration of the ovarian response to the administration of human menopausal gonadotrophin. Without it being possible to exclude any direct effect of prolactin on the ovary, it may be affirmed that the hormone decreases the sensitivity of the gonadotrophic cells to the positive feedback mechanism exerted by plasma estradiol.

Adult↗
PubMed1977

[The effect of several sexual steroids, 2-bromo-ergokryptin and lisurid-hydrogenmaleate an the postpartum concentration of serum prolactin and lactation (author's transl)].

The effect of Ablacton, Estrovis 4000, 2 Brom-alpha-ergokryptin (Cb 154) and of Lisurid-hydrogenmaleate (LHM) on lactation and the serum concentration of prolactin postpartum was studied. 10 normal nursing postpartum patients served as control. LHM was tested in a double blind study compared to placebo. The serum prolactin (PRL) was determined daily for the first 10 postpartum days by radioimmunoassay. Inhibition of lactation was consistent with Cb 154 (89% of the cases). Within two to three days after the onset of treatment with Cb 154 the changes of pregnancy in the breasts had completely subsided. The sexual steroids resulted in inhibition of lactation in 60% of the postpartum patients but mastodynia continued. LHM showed no difference from group taking placebo. The serum prolactin levels postpartum remained as high as a nursing mother's or rose with the administration of steroids. The administration of Cb 154 resulted in a drop of the serum prolactin to non-pregnant levels with in 2 days. The serum prolactin levels under treatment with LHM were not different from the group slowly. In nursing mothers, the stimulus of suckling maintain the pituitary secretion of prolactin as showed by higher serum prolactin levels and a slower decreased to normals than in the non-nursing mothers.

Bromocriptine↗
PubMed1987

Heterogeneous distribution of serum prolactin values in apparently healthy young women, and the effects of oral contraceptive medication.

Controversy over effects of oral contraceptives (OCs) on serum prolactin (PRL) levels from retrospective studies suggested performing a prospective study. Statistical analyses of PRL levels in 552 reproductive-age, nonmedicated women indicated a provisionally lognormal distribution of values less than 15 ng/ml, contaminated by a small number of abnormally high values less than or equal to 90 mg/ml. Truncated samples were used to estimate a "normal range" of PRL levels for three subsets of the study sample, classified according to number of weeks after pregnancy. Fifty-microgram estrogen-containing OCs doubled basal PRL levels at 5 to 8 weeks in those whose initial control values fell below 15 ng/ml, but the PRL elevation was no longer evident at 6 months of drug use. These OCs induced a small but significant lowering of PRL at 5 to 8 weeks in those with control levels of 15 ng/ml or higher. Thirty-five-microgram estrogen-containing OCs failed to alter PRL levels at 5 to 8 weeks in those with control values less than 15 ng/ml.

Age Factors↗
PubMed1979

Inherent ranges of seminal prolactin in pre- and postvasectomy subjects.

Seminal immunoreactive prolactin (i prolactin) was studied in 14 healthy subjects, ages 31 +/- 2 SEM, before and after undergoing elective vassectomy for birth control. Seminal plasma was separated within 2 hours of ejaculation, and prolactin was measured in duplicate by radioimmunoassay. The difference between the prevasectomy (mean +/- SEM 11.1 +/- 0.8 ng/ml) and postvasectomy seminal i prolactin (mean +/- 9.9 +/- 0.7 ng/ml) was statistically significant (mean +/- SEM 1.21 +/- 0.53 ng/ml, paired t-test, t = 2.36, P < 0.05). The mean prevasectomy seminal prolactin correlated with the corresponding mean postvasectomy value of the same subject (linear regression analyses, r = 0.77, P < 0.001). This study suggested that the accessory sex organs were the major source of seminal immunoreactive prolactin, and that a minor contribution might come from the in vivo presence of spermatozoa and/or testicular secretions. It also suggested that the magnitude of seminal immunoreactive prolactin was characteristic for each individual.

Adult↗