Showing papers on "Prolactin published in 1978"

Prolactin-screening tumors and hypogonadism in 22 men.

Abstract: We studied 22 men with prolactin-secreting pituitary tumors and hypogonadism. Twenty complained of impotence, nine had visual impairment, and three experienced galactorrhea. None of the 17 patients undergoing operation or radiotherapy, or both, were subsequently normoprolactinemic. In all 13 patients treated with bromocryptine major clinical improvement was associated with a decrease in serum prolactin levels and in nine with an increase in serum testosterone. Two patients receiving testosterone replacement therapy showed improved potency only after bromocryptine was administered. The results indicate that hyperprolactinemia frequently induces hypogonadism in men, that bromocryptine ameliorates symptoms of disease previously unchanged by operation or radiotherapy, and that the impotence observed may not be solely the result of hypogonadism.

Potent antidopaminergic activity of estradiol at the pituitary level on prolactin release

Abstract: Prior incubation of rat anterior pituitary cells with 17beta-estradiol led to an almost complete reversal of the inhibitory effect of two dopamine agonists, dihydroergocornine and RU 24213, on both basal prolactin release and thyrotropin releasing hormone-induced prolactin release. These experiments thus demonstrate a direct interference of dopamine action by a peripheral hormone. Prolactin secretion by pituitary cells in primary culture could possibly serve as an easily accessible model of a system under dopaminergic control.

Prolactin Release by Vasoactive Intestinal Polypeptide in Rats

Abstract: Synthetic vasoactive intestinal polypeptide (VIP) administered either intraventricularly or iv caused a significant and dose-related increase in plasma PRL levels in urethane-anesthetized rats. The administration of naloxone, an opiate receptor antagonist, significantly blunted the plasma PRL response to VIP. Increases in plasma PRL induced by VIP were also significantly suppressed by L-dopa, a precursor of dopamine, whereas pilocarpine, a cholinergic agonist, diphenhydramine, a histamine antagonist, and cyproheptadine, an antiserotoninergic agent, did not affect the plasma PRL response to VIP. In in vitro experiments, VIP alone did not stimulate PRL release from cultured pituitary cells, but it significantly attenuated the inhibitory action of dopamine, which was not blocked by naloxone. These results suggest that VIP stimulates rat PRL secretion, at least in part, through activation of an opiate receptor in the central nervous system and by blocking the inhibitory action of a dopaminergic mechanism at t...

Dopamine Levels in Hypophysial Stalk Blood in the Rat are Sufficient to Inhibit Prolactin Secretion In Vivo

Abstract: Much evidence indicates that dopamine can inhibit PRL secretion However, it is still unclear whether dopamine acts on hypothalamic neurons to stimulate PRL-inhibiting factor (PIF) release or whether dopamine is itself PIF, acting directly on the pituitary This study was designed to determine if PRL secretion is inhibited by dopamine infusions producing plasma dopamine levels which mimic those found in hypophysial stalk plasma Stalk plasma dopamine concentration in urethane-anesthetized diestrus-1 rats was 60 ± 11 ng/ml (mean ± SE; n = 10) During a dopamine infusion, stalk plasma dopamine levels were 70% of arterial levels Therefore, dopamine was infused at a rate which achieved arterial levels of 9–10 ng/ml and the effect on PRL secretion in urethane-anesthetized female rats was measured In diestrus rats, dopamine did not inhibit PRL secretion In rats pretreated with α-methyl-p-tyrosine to elevate serum PRL levels, dopamine suppressed PRL secretion 70% In rats with PRL levels elevated by median

Effects of a single injection of estradiol valerate on the hypothalamic arcuate nucleus and on reproductive function in the female rat.

Abstract: Young adult cyclic female rats were each injected with 2 mg estradiol valerate (EV) in sesame oil. Controls received an equivalent volume of sesame oil. Within 2 months after injection, most of the EV-treated animals showed persistent vaginal estrus and small polyfollicular ovaries as well as pathological changes in the hypothalamic arcuate nucleus. This pathological process was gradually progressive such that by 6 months after EV injection, the basal lateral region of the nucleus contained numerous reactive microglia, astrocytes, and degenerating elements of the neuropil. The experimental rats had elevated plasma PRL and GH concentrations which gradually diminished. Plasma estradiol concentration remained elevated 2 months after injection, while plasma LH and FSH concentrations stayed within the high and low normal range, respectively. The pituitary glands of injected animals weighed significantly more than those of controls 5.5 months after injection, but the enlarged glands did not cause hypothalamic compression. As mechanical anterior deafferentation of the medial basal hypothalamus has previously been shown to produce similar endocrine and reproductive alterations, it may be that estradiol treatment results in a functional-anatomical disconnection of the arcuate nucleus from the more anterior hypothalamic areas that regulate cyclicity. Whether this type of functional-anatomical phenomenon underlies other varieties of induced or secondary acyclicity in females remains to be determined.

Prolactin, growth hormone, and luteinizing hormone in the maintenance of testicular luteinizing hormone receptors.

Abstract: To elucidate further pituitary influence on testicular function, we studied the effect of PRL, GH, and LH alone or in various combinations on the maintenance of testicular LH receptor concentration and testosterone synthesis in response to LH (testicular responsiveness) in hypophysectomized adult rats. Hypophysectomy reduced LH receptor concentration by 80% and testicular responsiveness to LH by 70% 7 days after surgery. Treatment with PRL (75 or 150 μg/day) or with GH (75 or 150 μg/day) initiated within 6 h after surgery and continued twice daily for 6 days partially prevented the loss of LH receptors. The effect of PRL (150 μg/day) plus GH (150 μg/day) on LH receptor concentration was additive. The combination of LH (5 μg/day), PRL, and GH prevented any loss of LH receptors after hypophysectomy. A positive effect of LH on its receptor occurred in the presence of PRL. Treatment of hypophysectomized rats with 5 /μg LH plus 150 /μg PRL enhanced the effect observed with PRL alone (1.31 pmol/testis vs. 1.68 ...

Prolactin, Growth Hormone, Luteinizing Hormone Receptors, and Seasonal Changes in Testicular Activity in the Golden Hamster*

Abstract: In adult male hamsters, 2 months of exposure to a short photoperiod (5 h of light: 19 h of darkness) caused testicular regression and a precipitous decline in plasma PRL, in agreement with earlier reports from other laboratories. Depressed release of PRL cannot be explained by a reduction in testicular steroidogenesis, because castration of males kept in a long photoperiod did not reduce PRL levels and administration of testosterone to males kept in a short photoperiod failed to reverse the decline in plasma PRL concentration. Treatment of such “regressed” animals with PRL, GH, or ectopic pituitary transplants stimulated growth of the testes and the accessory reproductive glands, increased the concentration of LH receptors in the testes, and elevated plasma testosterone levels. A single injection of 250 μg PRL was sufficient to increase testicular LH binding, and chronic treatment with pituitary grafts completely reversed testicular regression. The effectiveness of exogenous PRL in stimulating testicular ...

Prolactin synthesis by human chorion-decidual tissue: a possible source of prolactin in the amniotic fluid

Abstract: Explants of human chorion-decidual tissue obtained at delivery from normal, full-term pregnancies synthesize and secrete prolactin. This hormone is indistinguishable from pituitary prolactin by chromatographic, electrophoretic, immunologic, and receptor assay techniques. These results suggest that chorion-decidua may be the source of the large quantities of prolactin in amniotic fluid.

Hyperprolactinaemia and impotence

Abstract: Clinical, laboratory and radiological findings were evaluated in twenty-nine men who had raised serum prolactin concentrations and pituitary tumours. Twenty-one had functionless pituitary tumours ('prolactinomas') and eight had acromegaly. Supraseller extension was detected in twenty of the twenty-six men who had lumbar airencephalography. Three patients were studied before, sixteen before and after and ten only after pituitary ablative therapy. Seventeen of these men complained of complete lack of libido and impotence and six had impaired libido and sexual potency; only six patients in this series denied reproductive symptoms. Thirteen of the impotent subjects had small soft testes, ten reduced facial and body hair and three had marked gynaecomastia. No features of hypogonadism were noted in the six patients without reproductive symptoms and none of the patients had galactorrhoea. Serum prolactin concentrations were higher and serum testosterone concentrations lower in the impotent men compared with those with normal sexual potency. Serum LH and FSH (both basal and in response to LHRH) oestradiol and oestrone concentrations were not different between the two groups and, except in those with post-operative hypopituitarism, were within the normal range. Following successful lowering of prolactin concentrations by surgery or bromocripitine or both, serum testosterone rose and potency returned; by contrast failure to lower prolactin concentrations was associated with persistent impotence and hypogonadism. The endocrine profile of low serum testosterone concentrations with gonadotrophins which had not risen into the range usually seen in primary hypogonadism (together with the parallel increase of LH and testosterone in one patient studied sequentially during treatment which suppressed prolactin levels to normal), suggested that the impaired gonadal function was caused by a prolactin-mediated disturbance of hypothalamic-pituitary function.

The arcuate nucleus and the control of gonadotropin and prolactin secretion in the female rhesus monkey (Macaca mulatta).

Abstract: Attempts were made to destroy selectively the arcuate nucleus with radiofrequency current in adult female rhesus monkeys as a first step in identifying the areas of the mediobasal hypothalamus (MBH) that are responsible for the neural control of gonadotropin secretion in this species. Extensive or complete destruction of the arcuate region was produced in three animals and in two of these the lesion was confined primarily to the arcuate region and the dorsal aspect of the posterior median eminence. These lesions resulted in the cessation of LH and FSH secretion and blocked the positive feedback action of estradiol on gonadotropin release but did not appear to influence grossly basal thyroid and adrenocortical function, or to abolish GH discharge in response to insulin hypoglycemia. Adenohypophysial infarcts were not observed and exogenous LHRH and TRH induced marked discharges of the appropriate anterior pituitary hormones. In two additional animals with large hypothalamic lesions, destruction of the arcuate region was incomplete. In this group only partial inhibition of gonadotropin secretion was observed. LH and FSH secretion did not appear to be influenced in one animal bearing a large MBH lesion that entirely spared the arcuate region. Although serum prolactin remained at pre-lesion control levels after placement of the two relatively discrete lesions confined to the arcuate region, unambiguous increases in the secretion of this hormone were observed when the area of destruction encompassed tissue anterior and/or dorsal to the arcuate region. These observations suggest that the arcuate region is the primary structure mediating the hypothalamic control of gonadotropin secretion in the rhesus monkey. They also suggest that, in this species, the regions of the MBH involved with the regulation of gonadotropin release and those which control prolactin secretion are anatomically distinct.

Prolactin Responses to Neuroleptics in Normal and Schizophrenic Subjects

Abstract: • The prolactin response to neuroleptics can serve as an index of dopamine blockade in humans. Plasma prolactin increments to single doses of chlorpromazine, and prolactin decrements to single doses of levodopa, were similar in normal and schizophrenic subjects. Antischizophrenic drugs of all chemical classes stimulated prolactin release, while chemically related drugs and other psychotropic agents ineffective in schizophrenia did not. The prolactin response to neuroleptic therapy occurred in all patients, and tolerance did not develop. Within subjects, prolactin responses were graded according to neuroleptic dose, but the upper limit of sensitivity of the response curve was achieved at doses below the therapeutic range. Relative prolactin-stimulating potency in humans of chlorpromazine, thioridazine, trifluoperazine, butaperazine, and haloperidol correlated well with their relative clinical potencies.

Estrogen control of prolactin synthesis in vitro

Abstract: Primary cultures of rat pituitary cells respond to estradiol-17beta by increased incorporation of radiolabeled precursors into prolactin but not into the bulk of other cellular proteins The rate of increase in prolactin synthesis is dose dependent, reaching maximal levels in the physiological range of estradiol At a concentration of 1 nM, estradiol, diethylstilbestrol, and estriol are stimulatory whereas androgens, progesterone, and corticosterone are without significant effect Exposure of pituitary cells to 10 nM estradiol resulted in a 500% increase in prolactin synthesis after 7 days of culture The results indicate that estradiol can stimulate prolactin synthesis through direct action on the pituitary

Effect of growth hormone on vitamin D metabolism.

Abstract: BEFORE affecting calcium and phosphorus metabolism, vitamin D3 (cholecalciferol) undergoes two hydroxylations; first in the liver, gut and perhaps other organs, to its major circulating form1,2 25(OH)D3 and then in the kidney3 to 1α,25(OH)2D3, the hormonal form. 1α,25(OH)2D3 is the most potent metabolite of cholecalciferol and may be chiefly responsible for all the effects of the vitamin on calcium metabolism4. Although the regulation of the secretion of 1α,25(OH)2D3 by the kidney has been a controversial subject, it is generally agreed that 1α,25(OH)2D3 itself5,6, the calcium and phosphorus content7–9 of the diet and parathyroid hormone (PTH)10 are all involved. But these factors do not seem adequate to account for the increased content of 1α,25(OH)2D3 in the plasma during growth spurts, pregnancy and lactation11, when the major increases in calcium and phosphorus absorption occur. We thought there might be a clue in the action of prolactin, which strongly increases the secretion of 1α,25(OH)2D3 in birds12,13 and enhances plasma 1α,25(OH)2D3 in lactating mammals14. Suppression of prolactin by administration of bromocriptine to lactating rats markedly lowers plasma 1α,25(OH)2D3 levels, although the drug has no such effect in non-lactating controls15. The similarity of the amino acid sequences of prolactin and growth hormone suggested that these hormones might have similar effects. We now report that administration to rats of a highly purified preparation of human growth hormone restores to normal the depressed plasma levels of 1α,25(OH)2D3 produced by hypophysectomy.

Hormonal induction of the secretory immune system in the mammary gland

Abstract: The secretory immune system of the mammary gland is undeveloped in virgin mice but becomes active at term and during lactation. This change appears to depend on migration to the mammary gland of precursors of IgA-secreting cells derived from the gut-associated lymphoid tissue, an origin which explains the specificity of milk IgA antibodies for enteric organisms. Because development of the epithelial components of the mammary gland is clearly under hormonal control, we examined the effect of mammotropic hormones on differentiation of the immune elements. Under a combined regimen of progesterone, estrogen, and prolactin, development of the glandular epithelium occurs with concomitant increments in the number of IgA-secreting plasma cells and amount of intraepithelial IgA. These increases appear to be due to enhanced capacity of the gland to attract or retain precursors of IgA plasma cells derived from gut-associated lymphoid tissue. Testosterone, which antagonizes lactation, also antagonizes development of the secretory immune system and decreases cellular trapping in the lactating gland. The ability of the gland to trap IgA immunoblasts is probably contingent upon a hormone-induced increase in receptors.

Selective Depression of Serum Growth Hormone During Maternal Deprivation in Rat Pups

Abstract: Maternal deprivation was associated with a decline in immunoreactive growth hormone in the serum of rat pups. Pups that were returned to the mother showed a rapid reversal in this deprivation-induced decrease. The change in growth hormone concentration was not accompanied by changes in the concentrations of prolactin, thyrotropin, or corticosterone in the serum, but were correlated with alteration in the activity of ornithine decarboxylase in the brain. Treatment of neonatal rat pups with cyprohepatadine, a serotonin antagonist that suppresses growth hormone secretion, resulted in a significant decline in both serum growth hormone concentration and brain ornithine decarboxylase activity. These findings suggest that maternal deprivation elicits a specific suppression of growth hormone release which mediates the decrease in ornithine decarboxylase activity. The study is consistent with clinical findings of impaired growth hormone "responsitivity" in human maternal deprivation syndrome.

Inhibition of gonadotropin and prolactin release by dopamine: effect of endogenous estradiol levels.

Abstract: The influence of endogenous estradiol (E2) levels on gonadotropin and PRL sensitivity to dopamine (DA) infusion (4 μg/kg/min) was assessed at different stages of the follicular phase of the menstrual cycle. Basal LH and FSH levels were comparable in day 2 and day 12 subjects, and despite a 4-fold increase in E2 concentration, the inhibition of LH by DA was small and quantitatively similar and there was no discernible effect on FSH in either group. In marked contrast, day 14 subjects with an elevated basal LH level exhibited a dramatic increase in the sensitivity of LH and FSH to DA inhibition. Further, a remarkable rebound release for LH but not FSH occurred on the termination of DA infusion. There was a significant correlation between basal LH and response to DA (r = 0.979). This unique increase in response to DA at a time when hypothalamic LRF secretion is assumed to be elevated suggests that DA may exert its effect by inhibiting LRF release. The inhibition of PRL release by DA is correlated with endoge...

Prolactin Binding Sites in the Rat Brain

Abstract: The principles of the competitive-binding assay were used in conjunction with light microscopic radioautography to demonstrate specific prolactin binding sites localized on ependyma of the rat choroid plexus, a previously unknown prolactin target tissue.

Release of growth hormone in lactating and non-lactating goats in relation to behaviour, stages of sleep, electroencephalograms, environmental stimuli and levels of prolactin, insulin, glucose and free fatty acids in the circulation

Abstract: Recording electrodes were implanted in contact with the dura mater overlying the parietal cortex of six female goats, four of which were lactating. After recovery from surgery and complete familiarization with the housing conditions, the personnel and the recording technique, each goat was observed continuously for 24 h with simultaneous recording of the cortical electroencephalogram (EEG). Remote blood sampling was carried out every 30 min without disturbing the animal. Apart from the release of growth hormone (GH) associated with morning milking in two of the goats, there was no consistent relationship between the apparently spontaneous, episodic release of GH and behvaiour, stages of sleep, cortical EEG, air temperature, time of day or night, obvious environmental stimuli which arose from the normal husbandry routine, or the levels of porlactin, insulin, glucose or free fatty acids in the blood. There was also no relationship between the release of prolactin and the stages of sleep.

The Effect of Thyrotropin-Releasing Hormone (TRH) and Somatostatin (GHRIH) on Growth Hormone and Prolactin Secretion in vitro and in vivo in the Domestic Fowl (Gallus domesticus)

Abstract: The effects of thyrotropin-releasing hormone (TRH) on growth hormone (GH) and prolactin (Prl) secretion have been investigated in vitro and in vivo in domestic fowl. In both conscious and anaesthetized immature chickens the administration (i.v.) of TRH (2.5 and 25 microgram/kg) significantly increased the concentration of plasma GH. The simultaneous administration of somatostatin (GHRIH), 2.5 microgram/kg, to conscious birds significantly reduced the magnitude of the GH response to TRH treatment, but had no effect on the basal levels of plasma GH. The repeated injection of TRH (10 microgram/kg) every 20 min over a 100-min period failed to maintain the concentration of plasma GH at a high level. Prl secretion was not stimulated in any of these experiments, and in anaesthetized birds TRH (2.5 and 25 microgram/kg) treatment was followed by a depression in the level of plasma Prl. The effects of TRH and GHRIH on GH secretion by an in vitro dispersed pituitary cell suspension system were very similar to the in vivo studies. TRH stimulated Prl release in vitro, in contrast to the in vivo studies, and the response was dose related. GHRIH had no effect on the basal release of Prl in vitro but significantly inhibited the response to TRH treatment.

Hormonal changes in serum in young men during prolonged physical strain.

Abstract: The endocrine response to severe physical strain including lack of sleep has been investigated in army personnel during a combat course of 5 days' duration. The thyroxine (T4) concentration in serum increased during the first 24 h, and then declined at a rate corresponding to a halflife of 7.6 days and on day 6 reached the lowest level, 55 ng/ml. Triiodothyronine (T3) displayed a similar pattern, although an increase during the first 24 h could not be demonstrated. Within 48 h after the course T4 had returned to normal, whereas the serum level of T3 was significantly below the level before the course (p<0.05). The serum level of TSH was suppressed during the course. The serum level of prolactin was significantly suppressed and growth hormone was markedly elevated during the course with a significant negative correlation (r=−0.6) between the two. In agreement with a previous report, there was a rapid and sustained suppression of the serum level of testosterone to a mean level of 1.1 ng/ml on day 5. Short periods of sleep (3–6 h) were shown to be effective in reversing the changes described in this paper, especially for growth hormone, prolactin, and testosterone.

Loss of Central Nervous System Component of Dopaminergic Inhibition of Prolactin Secretion in Patients with Prolactin-Secreting Pituitary Tumors

Abstract: A B S T RA C T The administration of L-dopa suppresses prolactin (PRL) secretion in normal subjects and in patients with hyperprolactinemia, although it is not known whether this effect, which requires the conversion of dopa to dopamine, is mediated peripherally or through the central nervous system. To distinguish between these effects, 10 normal subjects (6 male, 4 female) and 8 patients with hyperprolactinemia associated with pituitary tumors were given L-dopa, 0.5 g alone, or 0.1 g after a 24-h pretreatment with carbidopa, 50 mg every 6 h, which produces peripheral dopa decarboxylase inhibition. Similar degrees of PRL suppression were observed in normal subjects (basal plasma PRL 13+2 ng/ml) after L-dopa alone (48±+4%) and after L-dopa plus carbidopa (58+6%). In patients with pituitary tumors and elevated plasma PRL (73+14 ng/ml), L-dopa alone led to PRL suppression comparable with that in normal subjects (47±+6%). However, L-dopa plus carbidopa resulted in only minimal suppression of plasma PRL (19+4%) which was significantly less than after L-dopa alone (P <0.001). Urinary homovanillic acid excretion, which reflected peripheral dopa decarboxylation was similar in controls and tumor patients after L-dopa both alone and after carbidopa pretreatment. Comparable suppression ofPRL levels in response to a dopamine infusion (4 jig/kg per min for 3 h) was observed in controls and tumor patients. The results indicate that although peripheral conversion of exogenous dopa to dopamine can suppress PRL secretion, in normals, the central nervous system conversion ofdopa to dopamine in the presence of peripheral dopa decarboxylase inhibition is sufficient to account for its PRL-suppressive effects. In contrast, patients This work was presented in part at the AFCR National

The Physiological Role of Thyrotropin-Releasing Hormone in the Regulation of Thyroid-Stimulating Hormone and Prolactin Secretion in the Rat

Abstract: The physiological role of thyrotropin-releasing hormone (TRH) in the regulation of thyrotropin (thyroid-stimulating hormone, TSH) and prolactin (Prl) secretion has been assumed but not proven. Stimulation of their release requires pharmacologic doses of TRH. Lesions of the hypothalamus usually induce an inhibition of TSH secretion and an increase in Prl. To determine whether TRH is essential for TSH and Prl secretion in the rat, 0.1 ml of TRH antiserum (TRH-Ab) or normal rabbit serum was administered to normal, thyroidectomized, cold-exposed, and proestrus rats through indwelling atrial catheter. Serum samples were obtained before and at frequent intervals thereafter. Serum TSH concentrations in normal, thyroidectomized, cold-exposed, and proestrus rats were not depressed in specimens obtained up to 24 h after injection of normal rabbit serum. In contrast, serum TSH was significantly decreased after the administration of TRH-Ab in all normal (basal, 41+/-8 muU/ml [mean+/-SE]; 30 min, 6+/-2; 45 min, 8+/-3; 75 min, 4+/-2); thyroidectomized (basal, 642+/-32 muU/ml; 30 min, 418+/-32; 60 min, 426+/-36; 120 min, 516+/-146); coldstressed (basal, 68+/-19 muU/ml; 30 min, 4+/-3; 180 min, 16+/-8); and proestrus (basal, 11 a.m., 57+/-10 muU/ml; 1 p.m., 20+/-3; 3 p.m., 13+/-4; 5 p.m., 19+/-3) rats. However, 0.1 ml of TRH-Ab had no effect on basal Prl concentrations in normal or thyroidectomized rats and did not prevent the Prl rise in rats exposed to cold (basal, 68+/-7 ng/ml; 15 min, 387+/-121; 30 min, 212+/-132; 60 min, 154+/-114), or the Prl surge observed on the afternoon of proestrus (basal 11 a.m., 23+/-2 ng/ml; 1 p.m., 189+/-55; 3 p.m., 1,490+/-260; 5 p.m., 1,570+/-286). These studies demonstrate that TRH is required for TSH secretion in the normal, cold-exposed and proestrus rat and contributes, at least in part, to TSH secretion in the hypothyroid rat, but is not required for Prl secretion in these states.