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Results for “hyperprolactinemia”

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PubMed2001

Multiple intracranial recurrent tumors with hyperprolactinemia combined with a parasellar malignant fibrous histiocytoma long after transfrontal surgery and irradiation to a pituitary adenoma.

We herein describe a 40-year-old woman with hyperprolactinemia, an empty sella and two extrasellar intracranial recurrent tumors which were revealed 23 years after the first transfrontal craniotomy and 18 years after the second transfrontal surgery and irradiation to a provable prolactin-producing pituitary macroadenoma. One recurrent tumor was in the right orbital apex causing right oculomotor nerve palsy, and the other tumor was in the right apex partispetrosae and foramen jugulare. Although her serum prolactin level decreased after the administration of bromocriptine mesilate, and the size of the two tumors remained unchanged, a malignant fibrous histiocytoma, which might have been induced by the irradiation 18 years before, grew rapidly in the right suprasellar-prepontine cistern to the right pedunculus cerebralis, leading to a poor prognosis. This case confirmed the importance of the life-lasting follow-up of pituitary adenomas treated with surgery and/or irradiation therapy. Not only ectopic recurrence of the primary tumor but also post-irradiation tumors may become apparent long after the removal of the primary tumor.

Adult↗

PubMed2004

Superior cervical ganglionectomy differentially modifies median eminence and anterior and mediobasal hypothalamic GABA content in male rats: effects of hyperprolactinemia.

This work was undertaken to analyze the changes in GABA concentrations in the anterior and mediobasal hypothalamus and in the median eminence after acute or chronic superior cervical ganglionectomy (SCGx), and whether high prolactin levels interfere with the effects of SCGx on GABA content. Acute but not chronic SCGx increased GABA content in all the areas studied, as compared to controls. The presence of a pituitary graft abolished the effects of acute SCGx in the median eminence and anterior hypothalamus, as compared to controls, but potentiated its effects in the mediobasal hypothalamus. Chronic SCGx increased GABA content in the mediobasal and anterior hypothalami, as compared to pituitary grafted controls. Acute SCGx decreased plasma prolactin and GH levels, but chronic surgery did not modify these hormone plasma levels. Acute SCGx increased plasma ACTH levels, whereas chronic SCGx did not modify them. Pituitary grafting increased circulating values of prolactin, ACTH and GH, as compared to controls. Acute SCGx did not modify plasma prolactin levels in grafted animals, although it increased plasma GH levels and decreased those of ACTH in this experimental group. Chronic SCGx further increased both plasma prolactin and GH levels, without modifying plasma ACTH levels. These results suggest that SCGx differentially modifies GABA content within the hypothalamus and median eminence. Induction of hyperprolactinemia in the neonatal age interferes with SCGx effects on both GABA content within the hypothalamus and median eminence and the secretory patterns of the pituitary hormones studied.

Animals↗

PubMed1986

Lack of demonstrable tumor growth in progressive hyperprolactinemia.

Prolactin has been regarded as an excellent tumor marker for patients harboring prolactinomas, and a significant rise in the basal prolactin level is generally regarded as being commensurate with tumor growth. This report describes a case in which the basal serum prolactin level rose from 250 ng/ml to 1,528 ng/ml over a 10-year follow-up period in the absence of definitive therapy. Three sequential contrast-enhanced direct coronal computed tomographic scans obtained over a four-year period failed to demonstrate any evidence of growth of the 5 mm microprolactinoma. Progressive hyperprolactinemia may not be synonymous with tumor growth in patients with microprolactinomas.

Adult↗

PubMed1985

Hyperprolactinemia: its electrophysiologic and pharmacologic effect on neurons of the ventromedial nucleus of the hypothalamus.

Extracellular action potentials were recorded from 691 neurons in the ventromedial hypothalamus (VMH) of urethane anesthetized female rats under acute and chronic sham-operated and hyperprolactinemic conditions. Hyperprolactinemia was produced by transplanting pituitaries under the kidney capsules. Neuronal excitability was recorded and analyzed during spontaneous, baseline activity and following the iontophoretic application of prolactin, dopamine (DA) and luteinizing hormone-releasing hormone (LH-RH). No statistically significant changes were observed in the spontaneous electrical activity of VMH neurons under the conditions tested. Of the responsive neurons, approximately 90% of the neurons recorded and tested with prolactin displayed an increase in firing activity while DA produced a decrease, independent of the endogenous plasma prolactin levels (basal or elevated). However, the response to LH-RH was modified in the chronic hyperprolactinemic animal. The predominant response of VMH neurons to LH-RH in acute sham-operated and hyperprolactinemic as well as in chronic sham-operated animals was one of inhibition, while in the chronic hyperprolactinemic animal, the application of LH-RH initiated excitation rather than inhibition. These results provide evidence that chronic (long-term) exposure to elevated prolactin levels is a sufficient stimulus to modify the neuronal response pattern of VMH nerve cells to iontophoretically applied LH-RH but not to prolactin nor to DA.

Action Potentials↗

PubMed1989

Hyperprolactinemia-induced modifications in vasoactive intestinal peptide binding site densities in the rat central nervous system and pituitary gland: evidence for an interaction between estradiol-17 beta and prolactin effects.

Hyperprolactinemia was induced in ovariectomized rats by implanting estradiol-17 beta pellets, grafting extrapituitaries, or by a combination of both treatments. Subsequently, the effect of increasing plasma prolactin levels on both central and pituitary receptors for vasoactive intestinal peptide (VIP), a neuropeptide known to stimulate prolactin release was investigated. The results obtained by quantitative autoradiography show that the density of VIP binding sites is modified in restricted areas of the central nervous system (striatum, several cortical, thalamic and limbic structures) and in the pituitary in hyperprolactinemic animals. The present results suggest that changes in plasma prolactin levels may control VIP receptor site density in both brain and pituitary. Moreover, direct effects of estradiol-17 beta and possible interactions between estradiol-17 beta and prolactin are observed on both brain and pituitary VIP binding sites.

Animals↗

PubMed1986

Hyperprolactinemia enhances LH-stimulated 4-ene-5 alpha-reductase activity but inhibits LH-induced 17-hydroxylase activity in testes of hypophysectomized immature rats.

Two pituitaries from 7-week old female rats (Sprague-Dawley strain) were grafted under the capsule of the left kidney of 21-day old male rat. The pituitary grafted and sham-operated rats were hypophysectomized at 27 days of age. The hypophysectomized rats, in groups of 4, were given daily injections of 9 micrograms NIAMDD-oLH-23 (minimum effective dose) or saline for 3 days starting from day 29. Testicular homogenates were incubated with [3H]progesterone or [14C]4-androstene-3,17-dione, and enzyme activities per testes were estimated. Testicular HCG-binding sites were also measured. Hypophysectomy caused significant decreases in activities of testicular 5 alpha-reductase, 17-hydroxylase, and 17 beta-hydroxysteroid oxidoreductase. These decreased enzyme activities were significantly stimulated by LH treatment. Although pituitary grafts alone showed no effects on these enzyme activities in the testes of the hypophysectomized rats, the grafts significantly enhanced LH-stimulated 5 alpha-reductase activities but inhibited LH-stimulated 17-hydroxylase activity. Testicular LH/HCG receptors were significantly increased by the grafts, especially in the presence of LH, without affecting affinity for HCG. The present results demonstrate for the first time that hyperprolactinemia directly stimulates LH-stimulated 5 alpha-reductase activity in rat testes. The results also show that the same grafts directly inhibit LH-stimulated 17-hydroxylase activity, probably via postreceptor mechanisms.

17-Hydroxysteroid Dehydrogenases↗

PubMed1991

Characterization of a new animal model of chronic hyperprolactinemia.

Animal models of chronic prolactin (PRL) excess have included rats bearing transplantable pituitary tumors that have produced other hypophyseal hormones in addition to PRL. We report characterization of a new model, the Buffalo rat implanted with the MMQ tumor, a line developed from the 7315a line. Rats implanted with the MMQ tumor have serum PRL levels that increase with time and correlate with the estimated volume of the subcutaneous tumor. When rats are killed 4 weeks after implantation, serum PRL levels are strikingly higher in tumor-bearing rats compared with controls (females, 2,723 +/- 266 v 192 +/- 46 ng/mL, P less than .0001; males, 1,637 +/- 213 v 99 +/- 11 ng/mL, P less than .0001). Serum PRL levels measured by the Nb2 lymphoma assay were higher than immunoassay measurements in both tumor-bearing and control Buffalo rats. Sephadex chromatography of serum from tumor-bearing rats showed that most of the PRL immunoreactivity co-eluted with 125I-rPRL. Neither serum growth hormone (GH) nor luteinizing hormone (LH) levels were different from controls in tumor-bearing rats. Female MMQ-bearing rats had lower estradiol levels. At death, the wet weights of adrenal glands, kidneys, and gonads were not affected by the presence of tumor. In contrast, tumor-bearing rats had increased spleen weight and histological evidence of white pulp hyperplasia. The Buffalo rat implanted with the PRL-only MMQ tumor is a promising new tool for the study of chronic hyperprolactinemia.

Animals↗

PubMed1991

Hypercalciuria in a new rat model of hyperprolactinemia.

Hypercalciuria has been reported in rats with mild hyperprolactinemia due to implantation of anterior pituitary glands under the kidney capsule and in rats bearing transplantable tumors that secrete large amounts of prolactin (PRL) and growth hormone (GH). We studied Buffalo rats implanted subcutaneously with the new MMQ pituitary tumor line that secretes only PRL. Urinary calcium excretion increased as the tumors grew. Three weeks after tumor implantation in female rats, the urinary calcium excretion was 1.102 +/- 0.092 mg/100 g body weight (BW).24 hours compared with controls, 0.296 +/- 0.079, P less than .0005. Male tumor-bearing rats also had increased urinary calcium excretion compared with male controls. In tumor-bearing rats the urinary calcium excretion factored for urinary sodium excretion, dietary calcium intake, or urinary creatinine excretion was elevated. Urinary calcium excretion was correlated with serum PRL levels and with estimated tumor volume. Serum calcium, immunoassayable parathyroid hormone, and urinary cyclic adenosine monophosphate (cAMP) excretion were normal in the tumor-bearing rats. There was some evidence of loss of bone calcium in rats bearing the MMQ tumor, and serum levels of calcitonin were decreased. These results are similar to those found in anterior pituitary-grafted hypercalciuric rats. It is unlikely that parathyroid hormone (PTH) abnormalities are responsible for the hypercalciuria in the MMQ-bearing rats. The pituitary gland may have an effect on the distal renal tubule to decrease calcium reabsorption.

Animals↗

PubMed1992

Primary amenorrhea-galactorrhea with hyperprolactinemia and huge pituitary enlargement in juvenile primary hypothyroidism.

We report a girl with juvenile primary hypothyroidism revealed by growth retardation and a syndrome of primary amenorrhea-galactorrhea with hyperprolactinemia and suprasellar pituitary enlargement. Resolution of the pituitary enlargement and the amenorrhea-galactorrhea syndrome occurred after thyroid hormone replacement. No similar observation has been reported earlier in juvenile hypothyroidism.

Adult↗

PubMed1986

Effects of sustained hyperprolactinemia induced by chronic treatment with domperidone on central dopaminergic systems in the rat.

Chronic treatment with Domperidone (DOM) had no effect on basal prolactin (PRL) secretion or basal levels of Dopamine (DA) metabolites in basal hypothalamus and striatum as compared with the vehicle treated rats. Animals chronically treated with DOM did not present tolerance to a challenge dose of Haloperidol (HAL) and DOM either measuring PRL secretion or striatal DA metabolite levels. The PRL-induced increase in hypothalamic 3,4-dihydroxyphenylacetic acid (DOPAC) was reduced. These results were accompanied by no change at striatal DA receptors, a slight reduction in density-affinity at hypothalamic DA receptors but clear-cut modification in pituitary DA receptors with the appearance of a high affinity-low capacity binding sites. It can be surmised that sustained hyperprolactinemia may induce tolerance in hypothalamic Tuberoinfundibular (TIDA) neurons involved in the inhibitory control of PRL secretion and a change in the kinetic properties of pituitary DA receptors, but it does not consistently affect the activity of the nigro-striatal DA system.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1985

Hyperprolactinemia and male sexual behavior: effects of steroid replacement with estrogen plus dihydrotestosterone.

To determine if alterations in the availability of the active metabolites of testosterone (T) are involved in the inhibition of sexual activity in hyperprolactinemic animals, the effects of four ectopic pituitary grafts on copulatory behavior were examined in castrated male rats given subcutaneous implants of T or estradiol-17 beta (E2) plus 5 alpha-dihydrotestosterone (DHT). Two weeks after implantation of the steroid-filled capsules, half the animals of each group were given pituitary grafts and the remainder were sham-operated. Tests of copulatory behavior were performed prior to, and one, two, and three months following pituitary transplantation. Pituitary grafting caused significant inhibition of copulatory behavior in both T and E2 + DHT treated animals. PRL levels were significantly higher in E2 + DHT treated grafted males than in T treated grafted animals (2000 +/- 140 vs. 395 +/- 26 ng/ml), but did not differ between the corresponding control groups (61 +/- 8 vs. 73 +/- 6 ng/ml). The results of these experiments preclude the possible involvement of alterations in steroid secretion by the testes or modifications of the conversion of T to its active metabolites in the effects of hyperprolactinemia on copulatory behavior.

Animals↗

PubMed1994

Immunocytochemical demonstration of prolactin interaction with choroid plexus in aging and acute hyperprolactinemia.

Prolactin (PRL) exerts a direct effect on the central nervous system, reaching the PRL-responsive brain regions via cerebro-spinal fluid (CSF). The hormone enters the CSF by a specific receptor-mediated transport mechanism that is localized on the epithelium of the choroid plexus (CP) of brain ventricles. PRL interactions with the CP in aging were examined in young (3-month) and old (27-month) female Wistar rats using immunocytochemistry (immunogold technique). The enhancement of PRL uptake by the CP in animals at both ages was achieved by the modelling of acute hyperprolactinemia. A great age-related difference was found in the intensity of immunocytochemical reaction under activated conditions, the uptake of PRL by CP being significantly higher in young animals than in old. The character of the colloidal gold particle distribution in different components of CP epithelial cells appeared to be the same in both age groups. The weakening of PRL-transporting capacity in the CP of old animals may constitute one aspect of the alteration of neuroendocrine regulation in the CP-CSF system that occurs during aging.

Acute Disease↗

PubMed1994

Anomalous growth hormone response to vasoactive intestinal peptide and peptide histidine methionine in patients with prolactinoma or hypothalamic hyperprolactinemia.

We examined a possible GH-releasing activity of vasoactive intestinal peptide (VIP) and its homologous peptide, peptide histidine methionine (PHM), in 22 patients with hyperprolactinemia (HPRL) who comprised 19 cases of prolactinoma (PRLoma) and 3 cases of hypothalamic HPRL. Each patient underwent iv bolus injections of VIP (100 micrograms) and PHM (100 micrograms) on separate days, and plasma levels of GH and PRL were measured. The plasma GH response to VIP and PHM were considered positive (a paradoxical increase) when an increase over baseline of at least 50% occurred. In agreement with previous reports, the PRL-releasing activity of VIP and PHM in our patients with HPRL were subnormal. Thirteen (59%) patients showed a paradoxical rise in GH after VIP, and 4 (18%) patients did so after PHM. It is to be noted that all the 3 patients with hypothalamic HPRL responded to VIP with a significant rise in GH. 3 of the 4 PHM-responders were also responsive to VIP, which suggests that PHM may have activated VIP receptors in the pituitary of the PHM-responders as a partial agonist of the VIP receptor. The responders and nonresponders to VIP or PHM, respectively, had similar results with respect to the mean age, and the mean basal PRL and GH levels in the plasma. Since these paradoxical GH responses were observed in not only the patients with PRLoma but also those with hypothalamic HPRL, it may be that these anomalous GH responses in HPRL were due to the HPRL itself rather than due to the neoplastic lactotrophs.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1991

Possible role of vasoactive intestinal peptide in the hyperprolactinemia induced by ethanol.

The effect of the blockade of endogenous VIP by injecting a specific rabbit anti-VIP serum (A-VIP) was studied in rats receiving an acute injection of ethanol. A-VIP administration decreased serum prolactin levels and reduced the hyperprolactinemia induced by ethanol. We also investigated the effect of the acute administration of ethanol on the concentration and release of VIP from the mediobasal hypothalamus. Ethanol decreased VIP concentration in the mediobasal hypothalamus, whereas it stimulated the in vitro K(+)-evoked release of VIP from this tissue. Conversely, ethanol increased VIP concentration in the anterior pituitary gland. The data indicate that VIP may be involved in the pituitary response to ethanol. The increased anterior pituitary VIP after ethanol may be due to an augmented release from the mediobasal hypothalamus.

Animals↗

PubMed1991

Tyrosine hydroxylase and POMC mRNA in the arcuate region are increased by castration and hyperprolactinemia.

We have examined the changes which occur in neuronal expression of tyrosine hydroxylase (TH) and proopiomelanocortin (POMC) mRNA in response to castration and hyperprolactinemia (HP) in male rats. Steady-state mRNA levels were determined by quantitative in situ hybridization histochemistry (ISHH) using 35S-labeled synthetic 48-base oligodeoxynucleotide probes. Castration produced a 27% increase in TH mRNA in the periventricular and arcuate nuclei. PRL-exposed rats exhibited a further 27% increase in the level of TH mRNA and a striking 48% increase in POMC mRNA in periarcuate region cell bodies. These results indicate that gonadal steroids and PRL are involved, either directly or indirectly, in regulating the biosynthesis of TH and POMC in the hypothalamus.

Analysis of Variance↗

PubMedDate not supplied

Effect of an antagonistic analog of LH-RH on haloperidol-induced hyperprolactinemia in female rats.

The effects of prolonged treatment with the antagonistic analog of LH-RH (N-Ac-D-p-Cl-Phe1,2, D-Trp3,D-Arg6,D-Ala10) LH-RH (ORG 30276) on the hyperprolactinemia induced by haloperidol were investigated in intact or ovariectomized female rats. Treatment with ORG 30276 for 20 days significantly reduced prolactin levels elevated by daily injections of haloperidol in intact as well as in ovariectomized rats. Administration of ORG 30276 also significantly decreased serum LH levels in both types of rats. It is concluded that the LH-RH antagonist ORG 30276 is able to counteract the hyperprolactinemic effect of haloperidol. This effect might be due to a blockade of the action of endogenous LH-RH on the gonadotrophs, which results in a suppressing of the paracrine action of these cells on the lactotroph.

Animals↗

PubMedDate not supplied

Effect of passive immunization against substance P in rats with hyperprolactinemia.

Substance P, an undecapeptide isolated from gut and brain tissues, was reported to stimulate prolactin release. It was suggested that substance P may play a role in the control of prolactin secretion. In this investigation we studied the effects of the blockade of endogenous substance P by the administration of a specific anti-substance P serum on serum prolactin levels in rats in the evening of proestrus, in lactating rats after suckling, and in male rats with hyperprolactinemia induced by grafting 2 anterior pituitary glands under the kidney capsule. The injection of the anti-substance P serum was followed by a significant decrease of the prolactin surge induced by 30 min suckling in lactating rats, when the antiserum was administered 24 hr but not 5.30 hr earlier. Anti-substance P serum also induced a significant decrease in serum prolactin levels in pituitary grafted rats, but induced no change in the proestrous surge of prolactin and LH. These results show that substance P may be involved in the release of prolactin induced by suckling and that this peptide may have an intrapituitary role in the process of prolactin release. On the other hand, substance P does not seem to play a significant role in the proestrous peak of prolactin and LH.

Animals↗

PubMed1987

Hyperprolactinemia reduces vasoactive intestinal peptide in the anterior pituitary glands of rats.

The concentration of vasoactive intestinal polypeptide (VIP) in the anterior pituitary gland of female rats was significantly reduced by pituitary implants, prolactin-secreting tumours or dopamine blockade-induced hyperprolactinemia. Oestradiol implants increased plasma prolactin (PRL) to 12 times and increased pituitary VIP to 3.5 times that of controls after one week. The dopamine agonist bromocriptine significantly reduced pituitary VIP at doses within the clinically used range. These results provide evidence for a suppressive effect of plasma PRL on pituitary VIP, which may be effected by a dopaminergic mechanism, but is over-ridden by oestrogen.

Animals↗