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At least 523 records · Page 29Linked to original sources
PubMed1976

Effect of acute increases in serum triiodothyronine on TSH and prolactin responses to TRH, and estimates of pituitary stores of TSH and prolactin in normal subjects and in patients with primary hypothyroidism.

Previous investigators have shown that daily administration of TRH to normal individuals leads to diminishing TSH responses which were believed due to rising serum T3 with subsequent feedback inhibition of the pituitary. Patients with primary hypothyroidism were examined in the present study to test this hypothesis, since their T3 cannot increase after TRH. Bi-daily TRH (100 mug) was given to 4 patients for 3 consecutive days, and repeated on a 4th day following oral T3 (50 mug). TSH and PRL responses were unchanged during these 3days of serial TRH and were unaltered by T3 administration on the fouth day. In 5 other hypothyroid subjects studied before and during 3 consecutive days of T3 administration, TSH but not PRL responses to TRH appeared to decrease slowly but progressively. These observations led us to re-examine TRH responses in normal subjects given T3, since other workers had reported that 50 mug T3 completely abolished TSH response. Responses to TRH in 11 normals on a control day were compared to those observed 1 hour after oral T3. In spite of marked increases in serum T3, there was no significant difference between the mean TSH responses of the two studies.

Clinical Trials as Topic↗
PubMed1978

Effects of prolactin and prolactin plus luteinizing hormone on plasma testosterone levels in normal adult men.

In an earlier study, normal adult men were shown to have increased plasma testosterone (T) levels over a several-hour period after haloperidol-induced increases in plasma PRL levels. The present study was designed both to replicate our first study and to examine the potential synergism of PRL and LH in influencing T levels on a short term basis in normal men. Eight volunteers received on 4 separate days an in injection of saline or 0.5 mg haloperidol at 1000 h and an iv injection of saline or 88 IU human LH (hLH) at 1100 h in a double blind randomized block design arranged to augment plasma levels of PRL, LH, and PRL and LH together on the different test days as well as to afford a saline control day. Only five of the eight subjects had prompt PRL responses to haloperidol equivalent to those of our earlier study. As the purpose of this study was to examine the effect of increased PRL on plasma T levels, these five subjects were used for the determination of changes in plasma T. After haloperidol administration, their PRL levels rose an average of 19 ng/ml, to the high-normal range, and after the hLH infusions, their LH levels rose an average of 71 ng/ml. On the saline control day, mean T levels showed the normal diurnal decline. After 0.5 mg haloperidol, T levels were maintained for several hours, and after 88 IU hLH, T levels were increased for several hours. Increased PRL levels concomitant with hLH administration did not produce a T response greater than that caused by hLH alone. The results of this study replicate the effect of drug-induced PRL augmentation on plasma T levels found in our earlier study, but they fail to demonstrate a synergistic effect of acutely increased PRL on LH-stimulated T secretion. PRL thus seems to be another pituitary hormone capable of increasing plasma T in adult men, but it clearly is a weaker stimulus than LH.

Adult↗
PubMed1978

Serum prolactin response to thyrotropin-releasing hormone and metoclopramide in patients with prolactin-secreting tumors before and after transsphenoidal surgery.

Seven female patients with amenorrhea, galactorrhea, and hyperprolactinemia were examined before and after selective transsphenoidal removal of a PRL-secreting microadenoma. Before adenomectomy, metoclopramide (MCP; 10 mg orally) and TRH (200 micrograms iv) did not increase PRL blood levels in any of the seven patients. On the contrary, after oral administration of 10 mg MCP, a positive response was noted in a group of eight lactating women 3 days postpartum. After surgery, serum PRL level returned to normal in all patients. A positive PRL response to MCP and TRH was found in six of the seven patients 1 month after surgery. One patient, who had the lowest PRL level, failed to show a PRL increase after both stimuli. These findings indicate that hypothalamic pituitary function can be restored to normal after transsphenoidal removal of PRL-secreting pituitary tumors.

Adenoma↗
PubMed1979

Circulating big human prolactin: conversion to small human prolactin by reduction of disulfide bonds.

The heterogeneity of circulating human PRL (hPRL) in sera of patients with hyperprolactinemia was studied by exclusion chromatography on Sephadex G-100. Big hPRL, which elutes between the void volume and the elution position of monomeric small hPRL, is stable upon rechromatography but is almost entirely converted into small hPRL after reduction with 0.5% mercaptoethanol. These results suggest that the existence of circulating big hPRL is dependent upon the formation of interpolypeptide disulfide bonds and does not represent a classical biosynthetic precursor of hPRL.

Adolescent↗
PubMed1984

Prolactin-secreting adenomas in women. VII. Dopamine regulation of prolactin secretion.

Previous studies demonstrated that high doses of dopamine administered as a constant infusion were capable of suppressing PRL secretion in both normal and hyperprolactinemic individuals. The present study was designed to examine the dose-response relationship of PRL suppression to low doses of dopamine (between 0.06 and 4 micrograms/kg X min) infused in a step-wise fashion. Ten hyperprolactinemic patients with PRL-secreting pituitary adenomas and 10 normally menstruating women in the early follicular phase of a cycle were studied. For hyperprolactinemic women, the mean (+/- SD) serum PRL level (by RIA) was 112 +/- 101 ng/ml, with a range of 26-386 ng/ml, the mean estradiol level (by RIA) was 28 +/- 8 pg/ml, and the mean baseline dopamine level by carboxy-o-methyl transferase assay (COMT) was 357 +/- 237 pg/ml (2.33 +/- 1.54 X 10(-9) M). The normal women had a mean PRL of 8.1 +/- 3.5 ng/ml, a mean estradiol level of 42 +/- 12 pg/ml, and a mean baseline dopamine level of 317 +/- 223 pg/ml (2.07 +/- 1.45 X 10(-9) M). Concentrations of dopamine achieved at the lowest doses infused were less than 10 times baseline levels and were in the nanomolar range. The measured IC50 (the concentration of dopamine required to achieve 50% of maximal suppression) was 6 +/- 3 X 10(-9) M for normal women and 14 +/- 4 X 10(-9) M for hyperprolactinemic patients. The apparent inhibition constant determined by a nonlinear least squares procedure, was 3 +/- 3 X 10(-9) M for normal women and 11 +/- 12 X 10(-9) M for women with hyperprolactinemia. Both groups exhibited dose-dependent suppression of PRL to about 80% of initial values. Under these experimental conditions, the data do not support the hypothesis that there is a marked loss in sensitivity to dopamine in patients with PRL-secreting adenomas.

Adenoma↗
PubMed1984

Twenty four-hour prolactin profiles and prolactin responses to dopamine in long distance running women.

Long distance women runners have a high incidence of oligoamenorrhea. In order to study the possible role of PRL in contributing to their menstrual dysfunction, we evaluated PRL secretion in eumenorrheic (n = 7) and oligomenorrheic runners (n = 9) who averaged 25-50 miles/week, as well as nonrunning women (n = 5) during the midfollicular phase of their cycles. Serum estradiol, progesterone, testosterone, FSH, LH, TSH, and T4 were similar among the three groups. The mean 24-h +/- SE PRL concentrations between the three groups: nonrunners, 12.9 +/- 0.6 ng/ml; eumenorrheic runners, 13.5 +/- 0.4 ng/ml; and oligomenorrheic runners, 15.0 +/- 0.8 ng/ml, were not significantly different. A dopamine (DA) infusion, 0.004 micrograms/kg X min, produced physiologic serum DA levels in these subjects. The nadir of serum PRL levels during DA infusion was similar in each group, which argues against an abnormality in dopaminergic tone in the runners with menstrual dysfunction. Our findings of normal 24-h PRL secretion and appropriate PRL responses to DA in women runners with menstrual dysfunction do not support a role for PRL in this disorder.

Adolescent↗
PubMed1985

Naloxone-induced prolactin secretion in women: evidence against a direct prolactin stimulatory effect of endogenous opioids.

Because both opioids and ovarian steroids influence PRL secretion, the relationship between these inputs to PRL control was investigated. Infusion of the opiate receptor antagonist naloxone (1.6 mg/h for 4-8 h) failed to alter serum PRL levels in hypogonadal women or normal women in the early follicular or late luteal phase. In contrast, a prompt and sustained naloxone-induced release of PRL was found in the late follicular and midluteal phases of the cycle, with maximum increments (mean +/- SE) of 16.9 +/- 5.3 and 9.7 +/- 3.2 ng/ml, respectively. In the luteal phase women, the number of PRL pulses was significantly (P less than 0.001) greater during naloxone than during saline infusion (3.4 vs. 1.6 pulses/8 h), and a positive linear correlation was found between the integrated PRL response to naloxone and the levels of circulating estradiol (r = 0.62) and progesterone (r = 0.95). When serum LH concentrations were determined in the same samples, a significantly (P less than 0.001) greater synchrony of PRL with LH pulses during naloxone infusion (96%) compared to that during saline infusion (36%) was found in the luteal phase women. Thus, naloxone infusion induced an increase in pulsatile PRL release which was synchronized with LH pulses. These findings, not previously reported, suggest that a common neuroendocrine mechanism is involved in the opioidergic control of PRL and LH secretion and that this effect of naloxone is manifested only during high ovarian steroid environments.

Endorphins↗
PubMed1986

Carbidopa plus L-dopa pretreatment inhibits the prolactin (PRL) response to thyrotropin-releasing hormone and thus cannot distinguish central from pituitary sites of prolactin stimulation.

Contrary to a previous report, pretreatment of normal men with carbidopa plus L-dopa (Sinemet 25/250) markedly inhibited the PRL response to TRH, a stimulus that acts directly on the pituitary. Thus, the results of carbidopa/L-dopa testing cannot be used to determine whether agents that stimulate PRL secretion act on the pituitary or at a higher central nervous system level.

Adult↗
PubMed1989

Circadian variation of basal plasma prolactin, prolactin response to suckling, and length of amenorrhea in nursing women.

The circadian pattern of plasma PRL levels and the PRL response to suckling were examined at various times during the first postpartum year and related to the length of lactational amenorrhea. Ten healthy women whose infants were breast-fed exclusively and who were amenorrheic 3 months postpartum were studied 3, 6, and 9-11 months postpartum. The women and their babies were admitted to a metabolic unit for 48 h. On the second day, blood samples were drawn at 2-h intervals for 26 h starting at 0800 h and also 10 and 30 min after the initiation of six of the nursing episodes. During the three postpartum periods, there was a circadian rhythm of basal plasma PRL concentrations; the peak concentrations occurred between 2400-0600 h. Suckling induced a significant rise in plasma PRL levels at all hours except 0800 h. There was a positive correlation between the duration of the nursing episode and the suckling-induced PRL increase at 30 min. Both the basal plasma PRL levels and the PRL responses to suckling diminished with time after delivery. This trend was less evident at 0400 h and was not fully explained by changes in the nursing pattern. The five women in whom menstrual cycles resumed before day 180 postpartum had lower basal and suckling-induced plasma PRL levels than the women who had amenorrhea for a longer period. This difference was present in the third month, when all women were amenorrheic and fully nursing and when the frequency and duration of nursing episodes and infant growth rates were similar. The results indicate that comparable nursing patterns may be associated with different plasma PRL levels, which are associated with different lengths of lactational amenorrhea. An early difference in the sensitivity of the breast-hypothalamus-pituitary system to suckling may explain the differences in the duration of lactational amenorrhea, which are not dependant on the breastfeeding pattern. The magnitude of the PRL response to suckling may predict the likelihood of recovering ovarian function during lactation.

Adult↗
PubMed1995

Some forms of big big prolactin behave as a complex of monomeric prolactin with an immunoglobulin G in patients with macroprolactinemia or prolactinoma.

The purpose of this study was to characterize the structure of big big PRL (bb-PRL) in patients with macroprolactinemia or prolactinomas. Serum samples from these patients were fractionated by Sephadex G-100 chromatography, and PRL was measured in the eluate by an immunoradiometric assay. The fractions containing bb-PRL were subjected to affinity chromatography with an antihuman immunoglobulin G (IgG) agarose column. PRL and IgG were assayed in the fractions obtained after affinity chromatography by immunoradiometric assay and radial immunodiffusion, respectively. bb-PRL was also immunoprecipitated with an antihuman PRL antibody, followed by polyacrylamide gel electrophoresis and Western blotting. We found that an average of 60% (range, 27-87%) of bb-PRL from patients with macroprolactinemia was retained by the agarose, indicating that this form of PRL contains an IgG. In one of the patients with prolactinoma, the big big form constituted 76% of the total PRL immunoreactivity. Most (75%) of the bb-PRL from this patient behaved as an IgG after affinity chromatography. In the two other patients with prolactinoma, we found that 22% and 25% of the bb-PRL, which represented only 2% and 3% of the total PRL in the serum, reacted as an IgG. In both groups of patients, the 23-kilodalton form of PRL was detected after the immunoprecipitation of bb-PRL. These results show that bb-PRL is in part a complex of 23-kilodalton PRL with an IgG and not an antibody mimicking the actions of PRL, as has been demonstrated for some large forms of growth-hormone.

Adenoma↗
PubMed1999

Expression cloning and characterization of PREB (prolactin regulatory element binding), a novel WD motif DNA-binding protein with a capacity to regulate prolactin promoter activity.

Previous studies have implied that a transcription factor(s) other than Pit-1 is involved in homeostatic regulation of PRL promoter activity via Pit-1-binding elements. One such element, 1P, was employed to clone from a rat pituitary cDNA expression library a novel 417-amino acid WD protein, designated PREB (PRL regulatory element binding) protein. PREB contains two PQ-rich potential transactivation domains, but no apparent DNA-binding motif, and exhibits sequence-specific binding to site 1P, to a site nonidentical to that for Pit-1. The PREB gene (or a related gene) is conserved, as an apparently single copy, in rat, human, fly, and yeast. A single approximately 1.9-kb PREB transcript accumulates in GH3 rat pituitary cells, to levels similar to Pit-1 mRNA. PREB transcripts were detected in all human tissues examined, but the observation of tissue-specific multiple transcript patterns suggests the possibility of tissue-specific alternative splicing. RT-PCR analysis of human brain tumor RNA samples suggested region-specific expression of PREB transcripts in brain. Western and immunocytochemical analysis implied that PREB accumulates specifically in GH3 cell nuclei. Transient transfection employing PREB-negative C6 rat glial cells showed that PREB is as active as, and additive with, Pit-1 in transactivation of a PRL promoter construct, and that PREB, but not Pit-1, can mediate transcriptional activation by protein kinase A (PKA). Expression in GH3 cells of a GAL4-PREB fusion protein both strongly transactivated a 5XGAL indicator construct and yielded a further stimulation of expression of this construct by coexpressed PKA, implying that PREB can mediate both basal and PKA-stimulated transcriptional responses in pituitary cells. These observations imply that PREB will prove to play a significant transcriptional regulatory role, both in the pituitary and in other organs in which transcripts of its gene are expressed.

Amino Acid Sequence↗