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PubMed1997

Natural and melatonin-stimulated changes in the circadian rhythm of prolactin secretion in the ewe during seasonal anestrus.

The relations between the circadian rhythms of melatonin and prolactin, and the effect of melatonin infused into the third ventricle or the mediobasal hypothalamus (MBH) on prolactin secretion and dopamine (DA) release were studied in anestrous ewes under increasing daylength conditions. The decreased amplitude and duration of nocturnal melatonin secretion were accompanied with changes in the daily pattern of prolactin secretion. Marked peaks of prolactin occurred after sunrise and melatonin decreases in February, as well as significant evening or nocturnal peaks under long day conditions between April and July. Melatonin infused into the third ventricle evoked an abrupt increase in the concentration of prolactin after 30 min, and the enhanced prolactin level was significantly higher than during the control infusion (range from 204 +/- 75 to 248 +/- 48 ng/ml vs. 128 +/- 68 to 149 +/- 93 ng/ml, mean +/- SD). The concentrations of DA in MBH perfusates decreased during perfusion of melatonin but to a degree similar to that noted in untreated ewes. These data suggest that short-term infusions of melatonin stimulate the secretion of prolactin in the ewe under increasing daylength conditions, and that this effect is not mediated by changes in DA release.

Anestrus↗
PubMed1976

Influence of cholinergic receptor blockade on drug-induced prolactin release in the monkey.

The influence of varying doses of perphenazine, thyrotropin-releasing hormone (TRH) and serotonin on prolactin release was examined in two species of monkeys: rhesus (Macaca mulatta) and crab-eating (Macaca fascicularis). The intravenous administration of 0.33 mg/kg body weight of perphenazine or 1.0 mug/kg body weight of TRH gave a greater release of prolactin than higher doses of perphenazine (1.0 mg/kg) or TRH) (3.4 mug/kg), respectively. Prolactin release induced by serotonin at doses of 1, 5 and 10 mug/kg was similar. Both atropine sulfate (Atr-SO4) and atropine methyl nitrate (Atr-MN) at a similar base level potentiated the prolactin releasing action of the high dose of perphenazine suggesting that high doses of perphenazine activate a cholinergic inhibitory component present in the pituitary. Atropine sulfate had no potentiating action on the TRH-induced prolactin release, while Atr-MN appeared to prolong the response of TRH without potentiating it. Neither form of atropine had any influence on serotonin-induced prolactin release. The data indicated that the lower prolactin response to high doses of perphenazine and TRH were brought about by different mechanisms, and that the mechanism for perphenazine appeared to be mediated through a pituitary cholinergic system.

Animals↗
PubMed1978

Effects of melatonin and natural and synthetic analogues of arginine vasotocin on plasma prolactin levels in adult male rats.

A significant elevation in plasma prolactin was observed 10 min following the intravenous injection of 100 microgram of melatonin into either estrogen-progesterone (EP) primed or into nonsteroid-treated male rats. 60 min postinjection in the EP primed rat, the groups treated with 100 microgram or 10 mg of melatonin had signficantly elevated plasma prolactin levels while no effect was observed with these same doses in the nonsteroid-treated rats. Compared to diluent-treated controls, a significant elevation in plasma prolactin was observed at 10, 20 and 60 min following the intravenous injection of either 1 microgram arginine vasotocin (AVT) or 1 mg melatonin into EP primed male rats. A consistent rise in plasma prolactin was also evident after the injection of 1 microgram of either arginine vasopressin, lysine vasopressin or AVT. Oxytocin had no effect on plasma prolactin values. The intravenous administration of 1 microgram of (deamino-1,6 dicarba, 8-arginine)-vasotocin caused a significant elevation of plasma prolactin 10 and 20 min after injection. However, the injection of another analogue of AVT, (4-leucine, 8-arginine)-vasotocin, had no effect on prolactin release at the time points measured.

Animals↗
PubMed1979

The suckling-induced rise of plasma prolactin in lactating rats: its dependence on stage of lactation and litter size.

The response of plasma prolactin in vigorous suckling was measured in lactating rats which had been isolated for 10-12 h from their offspring. Plasma prolactin was investigated during suckling at various stages of lactation. The results demonstrate that prolactin responds maximally to suckling already in the first days of lactation. In the second half of the lactation period, the prolactin rise in the plasma induced by suckling decreases gradually; this is not due to a reduced suck-intensity of older pups. A relationship is found between the height of the suckling-induced prolactin rise and litter size. The data suggest that during suckling in the first weeks of lactation the pituitary secretes large amounts of prolactin at a constant rate. It is speculated that in the first minutes of suckling, receptors may clear considerable amounts of released prolactin from the circulation.

Age Factors↗
PubMed1981

Effect of various concentrations of prolactin and growth hormone on the magnitude of stimulation of RNA synthesis, casein synthesis and ornithine decarboxylase activity in mouse mammary gland explants.

The effects of various concentrations of prolactin and growth hormone on the rates of [3H]-uridine incorporation into RNA, [3H]-leucine incorporation into casein, and ornithine decarboxylase (ODC) activity were determined in mouse mammary gland explants. The lowest concentrations of prolactin which produced significant responses were between 5 and 25 ng/ml. Growth hormone, in contrast, produced significant response at concentrations between 250 and 1,000 ng/ml. The prolactin actions on RNA and casein synthesis were essentially all-or-none type responses, i.e. the magnitude of the responses were maximal at about 10 ng/ml prolactin. The action of prolactin on ODC activity was quite different; a concentration-response relationship was observed with prolactin at concentrations from 10 t 250 ng/ml. It is apparent from these studies that different concentrations of prolactin are required to produce optimal actions on different biochemical parameters in cultured mammary tissues.

Animals↗
PubMed1995

Effects of the gonadotropin-releasing-hormone agonist, D-Trp-6-GnRH, on prolactin secretion in healthy young men.

The objective of this study was to examine the changes in basal plasma gonadotropin, alpha-subunit, sex steroids, and prolactin levels and the prolactin and luteinizing hormone (LH) secretion pattern before, during and 161 days after treatment with a depot preparation of D-Trp-6-GnRH in young men. Gonadotropins, alpha-subunit, sex steroids, and prolactin were measured in pooled plasma samples. Additionally, before treatment, several times during its course and on day 161 after treatment, blood samples were drawn for 8 h every 15 min for prolactin and LH measurements. After initial stimulation of the pituitary, administration of a depot preparation of D-Trp-6-GnRH resulted in a constant decrease in gonadotropin and sex steroid concentrations with LH and testosterone concentrations remaining within the limits of prepubertal levels from days 16 to 48. Alpha-Subunit concentrations (0.4 +/- 0.09 IU/l; mean +/- SE) increased after application of D-Trp-6-GnRH, and remained elevated until day 48. Basal prolactin levels (3.5 +/- 0.25 microgram/l) did not change significantly during treatment but afterwards increased consistently with maximal levels at day 141 (15.3 +/- 3.8 microgram/l); they had decreased at day 161 to 10.3 +/- 1.8 microgram/l which is significantly higher than before treatment (p < 0.05). On day 161, prolactin pulse amplitude was significantly higher than before and during treatment (p<0.05), while no significant changes in pulse frequency occurred. No significant temporal coupling between LH and prolactin release could be detected.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1978

Prolactin secretion in nonalcoholic liver cirrhosis.

Serum prolactin levels were determined following stimulation by sulpiride in 20 patients with nonalcoholic liver cirrhosis and 10 normal controls. Prolactin response was essentially the same in the two groups. Only 5 cirrhotics, all with ascites, showed a lower prolactin response after sulpiride stimulation. This was interpreted as a consequence of a rapid prolactin escape from blood into the ascitic fluid, as it was shown to be the case in 2 of these patients. It is concluded that prolactin secretion in nonalcoholic liver cirrhosis is essentially normal. The higher prolactin levels found by others in alcoholic cirrhosis could be the result of a direct effect of alcohol on hypothalamic structures involved in prolactin secretion.

Adult↗
PubMedDate not supplied

Blood pressure and prolactin: effects of guanfacine. Three-year follow-up study.

Serum prolactin was measured in 76 patients with essential hypertension: 47.4% had elevated serum prolactin, and those with organ damage had presented higher prolactin than those with Phase I (WHO) hypertension. The effect of prolonged treatment (3 years) with guanfacine, an alpha-adrenoceptor stimulant drug, on blood pressure levels, heart rate, and prolactin was evaluated in 15 patients with moderate essential hypertension (WHO: Phase II) and hyperprolactinemia. Treatment produced a marked reduction in blood pressure levels and heart rate. Guanfacine decreased serum prolactin significantly (p less than 0.001), and the inhibition persisted during the 3-year follow-up. The daily dosage of guanfacine did not have to be changed during the 3 years of treatment. Side effects of guanfacine were only observed during the first 3-4 months of therapy. The hypotensive effect of guanfacine was increased by the administration of a diuretic, a vasodilator, or a beta-adrenergic blocking drug. The results indicate that guanfacine administered alone or in combination is an effective drug for treatment of patients with essential hypertension. The inhibitory effect of guanfacine on prolactin suggests that hypothalamic or extrahypothalamic adrenergic pathways may participate in the regulation of prolactin secretion.

Adult↗
PubMed1981

Pituitary oligopeptide regulation of phosphatidylcholine synthesis by fetal rabbit lung cells: lack of effect with prolactin.

Phosphatidylcholine (PC) synthesis in cultured fetal rabbit lung cells was studied after exposure to various pituitary peptides. Because of reports of an association between lung maturation and prolactin, 2 different preparations of ovine prolactin were studied in concentrations ranging from 0.1 to 10.0 microgram/ml. Increased saturated phosphatidylcholine (SPC) synthesis without an increase in synthesis of total PC, and increased SPC/PC, was observed after exposure to Sigma prolactin. NIH prolactin in the same concentrations had no effect on synthesis of either PC or SPC. Adrenocorticotropic hormone, luteinizing hormone and thyroid stimulating hormone increased synthesis of both PC and SPC, but none increased the SPC/PC ratio. A cold ethanol extraction of Sigma prolactin yielded fractions with no demonstrable biologic activity, and other initial attempts to characterize the active factor in the Sigma prolactin samples were unsuccessful. We concluded that prolactin per se has no direct effect on PC or SPC synthesis in the lung, but that certain other pituitary peptides have a direct effect on lung synthesis of PC and SPC.

Adrenocorticotropic Hormone↗
PubMed1973

Thyroid hormone inhibition of the prolactin response to thyrotropin-releasing hormone.

The influence of serum triiodothyronine (T(3)) and thyroxine (T(4)) concentrations on the release of prolactin in man was studied by determining the prolactin response to synthetic thyrotropin-releasing hormone (TRH) in hypothyroid and hyperthyroid patients before and after correction of their serum thyroid hormone abnormalities. The maximum increment in serum prolactin above the basal level (maximum Delta prolactin) was used as the index of response to TRH. In 12 patients with primary hypothyroidism, the maximum Delta prolactin in response to TRH fell from 100.5+/-29.1 ng/ml (mean +/-SEM) before treatment to 36.1+/-6.0 ng/ml (P < 0.01) during the 4th wk of treatment with 30 mug T(3) + 120 mug T(4) daily. The mean serum T(3) level increased from 57+/-8 to 138+/-10 ng/100 ml, and the mean serum T(4) level increased from 3.0+/-0.4 to 7.2+/-0.4 mug/100 ml during this treatment. In eight normal subjects the maximum Deltaprolactin in response to TRH was not significantly different during the 4th wk of treatment with 30 mug T(3) + 120 mug T(4) daily from the response before treatment. In 10 patients with hyperthyroidism, the maximum Deltaprolactin in response to TRH increased from 14.2+/-2.9 ng/ml before treatment to 46.9+/-6.7 ng/ml (P < 0.001) during antithyroid treatment. The mean serum T(3) level fell from 313+/-47 to 90+/-8 ng/100 ml, and the mean serum T(4) level fell from 20.8+/-2.5 to 6.8+/-0.6 mug/100 ml during this treatment. These results show that changes from normal serum levels of T(3) and T(4) are associated with changes in prolactin responses to TRH; subnormal serum levels of T(3) and T(4) increase TRH-induced prolactin release, whereas substantially higher than normal serum levels of T(3) and T(4) inhibit this release.

Adolescent↗
PubMed1986

Assays for prolactin: guidelines for the provision of a clinical biochemistry service.

This paper summarises the views of the authors on the provision of a prolactin assay service. We discuss the pathophysiology of prolactin secretion and the clinical indications that arise from that. We cover the rather complex issue of the definition of normal and elevated prolactin levels. From these considerations, certain guidelines on the analytical performance of prolactin assays and their provision in a clinical biochemistry service are given. The extent to which currently available methods and performance as revealed by the UK External Quality Assessment Scheme (EQAS) match these guidelines are described and certain conclusions are reached. Finally, probable future developments are briefly discussed. The main conclusions and recommendations are as follows: Reagents of appropriate quality are available to enable prolactin immunoassays to be provided in UK clinical biochemistry laboratories. These are provided either separately or in the form of kits from both commercial and NHS sources. There is no requirement for individual laboratories to undertake their own antiserum production or prolactin iodination. Acceptable performance (as defined using internal QC procedures and the UK EQAS) is achievable using these reagents/kits, although one commercial kit shows a consistent marked negative bias. Reference ranges, including 'normal ranges', show considerable between-centre variability. Many centres have not established their own ranges, even those using in-house methods. Reference ranges for use in clinical biochemistry laboratories are proposed in this report. Some general guidance on the provision of a prolactin service is given, although this does not differ in principle from that appropriate for other peptide hormone analytes. There is no evidence that centres with small workloads perform any worse than average, although it may be more cost-efficient for such centres to send the samples elsewhere. As with other peptide analytes, non-isotopic immunometric methodology is likely to replace current radioimmunoassay methods in the near future.

Female↗
PubMed2003

The prolactin response to fenfluramine in depression: effects of melancholia and baseline cortisol.

Depression may be associated with a hypofunction of central serotonergic systems. The prolactin response to fenfluramine, an indicator of serotonergic activity, has been reported to be blunted in depressed patients compared to controls. It has also been suggested that blunting is more likely in melancholic depression. Baseline cortisol, prolactin and tryptophan availability have also been suggested to affect this response. Forty-eight men and 61 women with a major depressive episode, and who were drug free, and 20 healthy control men underwent clinical evaluation and fenfluramine challenge with dl-fenfluramine 1 mg/kg. When baseline variables were covaried, there was no difference in prolactin response to fenfluramine between males with depression and age-matched controls. Amongst all the depressed patients, body mass index showed a significant association with prolactin response to fenfluramine. There was an interaction between baseline cortisol and DSM-III-R melancholic subtype of depression whereby non-melancholic patients appeared more likely to increase prolactin response to fenfluramine in response to higher cortisol levels. Prolactin response to fenfluramine was not blunted in major depression and there was no difference between melancholic and non-melancholic depression. However, the relationship between prolactin response to fenfluramine and baseline cortisol levels appeared to differ between these two subtypes of depression.

Adolescent↗
PubMed2001

Prolactin in murine systemic lupus erythematosus.

Murine systemic lupus erythematosus (SLE) manifests several autoimmune perturbations that resemble human SLE, including cytokine aberrations, lymphoproliferation, hypergammaglobulinemia, autoantibody formation, and immune complex glomerulonephritis. In multiple studies, elevated serum prolactin concentrations (hyperprolactinemia) stimulated appearance or progression of murine lupus. Autoimmune disease acceleration by prolactin appears to be accentuated by estrogen stimulation of prolactin secretion and independent of immunosuppressive effects of androgens such as testosterone. Conversely, suppression of serum prolactin concentrations by bromocriptine inhibits development of murine SLE. These data clearly support the concept that prolactin is immunostimulatory in autoimmune disease and that the therapeutic goal of lowering serum prolactin concentrations may be beneficial to patients. Further utilization of murine SLE models will facilitate dissection of the actions and interactions of prolactin with estrogen, progesterone and testosterone and lead to a better understanding of hormonal immunomodulation and therapy of autoimmune disease.

Animals↗
PubMed1977

Evidence for a role of prolactin in prostate and seminal vesicle growth in immature male rats.

To determine if prolactin secreted endogenously by anterior pituitary grafts could augment male accessory organ weights, single anterior pituitary grafts were placed under the kidney capsule of male rats, whereas control animals received a graft of muscle. Three weeks after transplantation, the animals were sacrificed by decapitation and a significant increase in plasma prolactin was observed, which was accompanied by a highly significant increase in the weights of seminal vesicles, ventral and dorsal prostates, and adrenals. To determine the importance of testicular steroids in the response, animals were castrated. The increases in prolactin, seminal vesicle and ventral and dorsal prostate weights still occurred whether or not a small dose of testosterone replacement therapy was employed. In the presence of the pituitary graft, adrenal weight usually increased in these animals as well. To rule out a requirement for adrenal steroids in the response, adrenalectomized-castrate animals were also studied, and the increases in prolactin and prostate weights still occurred although there was no significant increase in the size of the seminal vesicles. To rule out the participation of other pituitary hormones, pituitary grafts were also placed in hypophysectomized animals, and in these animals, there was also a significant increase in prolactin, accessory sex organ and testicular weights, but the adrenals did not increase in size. The grafts failed to alter gonadotropin titers in any experiment. It is concluded that single anterior pituitary grafts are capable of secreting sufficient prolactin to increase the size of the sex accessories and sometimes the testes and adrenals of the rat. Furthermore, the effects on the male sex accessory organs were demonstrable in the absence of testicular or both testicular and adrenal steroids. The data suggest that prolactin may play a physiological role in the growth of the testes, adrenals and sex accessories.

Adrenalectomy↗
PubMed1977

Modification of serum luteinizing hormone and prolactin concentrations by corticotropin and adrenalectomy in ovariectomized rats.

The effects of ACTH and adrenalectomy (ADX) on serum concentrations of LH and prolactin were examined in ovariectomized (OVX) rats. In the first study ACTH (4 IU) was administered daily for one week. ACTH prevented an increase in serum LH in response to OVX and stimulated serum prolactin. ACTH also reduced serum LH in OVX+ADX rats and increased prolactin concentration. ADX was utilized in the second experiment to enhance secretion of endogenous ACTH. Two weeks after ADX serum prolactin was elevated above intact values. ADX also enhanced serum prolactin in OVX rats to the level found in intact animals. ADX markedly reduced the LH response to OVX but ADX alone had no effect on serum LH concentration. All of these findings indicate that ACTH acts directly to reduce serum LH concentration and to enhance serum prolactin. The influence of adrenal corticoids on serum concentrations of LH and prolactin as reported by other investigators appears to be mediated via their negative feedback effects on ACTH release. Whether ACTH has its action on adenohypophyseal cells or on hypothalamic sites has yet to be determined.

Adrenalectomy↗
PubMed1991

Free alpha molecules from pregnancy stimulate secretion of prolactin from human decidual cells: a novel function for free alpha in pregnancy.

Free alpha molecules isolated from pregnancy, as well as highly purified reference preparations of hCG alpha subunit (CR119 or CR123), stimulated the release of prolactin from human decidual cells in culture. The amount of prolactin secreted during a 24 h incubation was concentration-dependent over a range of increasing doses of alpha from 0.2 to 20 ng/ml with an ED50 of about 1.6 ng/ml. These concentrations are well within the physiologic maternal serum free alpha levels which average 350 ng/ml during the third trimester of pregnancy. Incubation of decidual cells with a reference preparation of intact hCG (CR123) at a concentration of 260 ng/ml resulted in stimulated secretion of prolactin, however, the observed stimulation could be attributed to contamination of the preparation with free alpha or dissociated hCG alpha subunit. Purified hCG beta subunit had no stimulatory activity on the decidual cell culture. The effect of alpha subunit on the stimulated release of prolactin was not due to a generalized stimulation of protein synthesis and secretion since no increase was observed in the release of 35S-labeled proteins compared to controls. In addition, the observed increase in prolactin secretion was not due to a toxic effect of the alpha subunit since there was no visible effect on cell viability, and the cellular enzymes, LDH and alkaline phosphatase, were not detected in the culture medium. Addition of exogenous hCG alpha subunit to primary cultures of human trophoblast cultures did not result in stimulated release of human placental lactogen. We conclude that free alpha molecules of pregnancy stimulate release of prolactin from human decidual cells in culture. These results suggest a novel role for free alpha in the paracrine regulation of decidual prolactin secretion.

Cells, Cultured↗
PubMed1976

The influence of cholinergic, adrenergic, and serotonergic drugs on the afternoon surge of plasma prolactin in ovariectomized, estrogen-treated rats.

The effects of systemic administration of cholinergic, adrenergic, and serotonergic drugs on the afternoon surge of plasma prolactin was investigated using ovariectomized, polyestradiol phosphate (PEP)-injected rats bearing aortic catheters. Basal prolactin levels were elevated and similar after PEP administration for a period of 5 weeks, and an afternoon surge in plasma prolactin persisted for a period of 3 weeks before the magnitude of the surge diminished. The plasma estradiol levels were significantly higher for the 1100 and 1300 h samples than for the 1500 and 1700 h samples. Cornified vaginal epithelia were predominant in the vaginal smears of all animals throughout the 49-day experimental period. The cholinergic agonists arecoline, nicotine, and carbachol significantly inhibited the afternoon surge of prolactin. The muscarinic antagonist atropine resulted in a partial inhibition of the surge while the nicotinic antagonist mecamylamine did not have any inhibitory effect. The alpha-adrenergic blockers phenoxybenzamine and phentolamine and the beta-blocker propranolol inhibited the prolactin surge, with phenoxybenzamine being most effective. The administration of the serotonergic antagonist methysergide resulted in only a partial blockade of the afternoon prolactin surge. The data suggest that both the adrenergic and serotonergic systems may have a positive input in the afternoon surge of plasma prolactin. It appears that the cholinergic system does not play a significant role in the afternoon surge.

Animals↗
PubMed1996

Prolactin receptor expression during adipocyte differentiation of bone marrow stroma.

To determine the role of the hormone prolactin and its receptor on the differentiation, growth, and metabolic activity of cells of bone marrow origin, prolactin receptor expression was assessed in bone marrow stromal cells. Using reverse transcription - polymerase chain reaction, BMS2 cells, a bone marrow stromal cell line, were shown to express prolactin receptors following adipocyte differentiation, using three different adipocyte-differentiation protocols. Primary bone marrow stromal cells also show a dose-dependent increase in prolactin receptor expression following treatment with adipogenic agonists. That prolactin receptor expression is inducible upon adipocyte differentiation was confirmed using a preadipocyte cell line 3T3 - L1. Further, prolactin receptor parallels lipoprotein lipase gene expression in 3T3-L1 cells. These results suggest that prolactin and its receptor may play a role in differentiation and/or metabolism of pre-adipocytes and adipocytes.

Adipocytes↗