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At least 235 records · Page 13Linked to original sources
PubMed1982

GABAergic control of anterior pituitary hormone secretion.

Anatomical and biochemical studies have identified a hypothalamic tubero-infundibular GABAergic system, which plays a functional role on anterior pituitary hormone secretion. Experimental and clinical evidence support the presence of a dual component in the action of GABA; one mediated via the central nervous system and the other exerted directly at the anterior pituitary level. The two sites of action may be responsible for the excitatory and inhibitory effects of GABA on pituitary hormone and especially prolactin secretion. The future characterization of this system will provide a better understanding of the involvement of GABA in the physiology of anterior pituitary hormone secretion and will contribute to the development of new pharmacological agents for the therapy of neuroendocrine disorders.

Adrenocorticotropic Hormone↗
PubMed1981

The isolation of human pituitary hormones from frozen glands.

An integrated scheme for the extraction and purification of human pituitary hormones from frozen glands has been developed. The method yields 6.3 mg/gland of monomeric pyrogen-free GH in a single fraction, with a potency of 2.5-3.1 IU/mg, as estimated by bioassay, radioreceptor assay, and RIA, with a further 0.6 mg/gland recovered from side fractions. A glycoprotein fraction yields 200 IU FSH, 500 IU LH, and 0.2 IU TSH per gland, as estimated by RIA. Additional hormones purified from side fractions include PRL, lipotropins, and the 20,000 molecular weight variant of human GH.

Chromatography, DEAE-Cellulose↗
PubMed1985

Further studies on the localization of angiotensin-II-like immunoreactivity in the anterior pituitary gland of the male rat, comparing various antisera to pituitary hormones and their specificity.

Using immunocytochemistry with the sensitive avidin-biotin complex method and an antibody to the beta subunit of rat luteinizing hormone (rat LH beta) provided by the National Hormone and Pituitary Program, NIADDK, to identify gonadotrops, the presence of angiotensin II-like immunoreactivity in the gonadotrops of the anterior pituitary gland of male rats was confirmed. However, using an antibody to rat prolactin, no angiotensin II-like immunoreactivity could be found in lactotrops. This finding is at variance with a previous report from this laboratory, in which the lactotrops were identified with an NIADDK antibody to human prolactin. The possibility that the antibodies to human prolactin cross-reacted with rat LH was therefore investigated by a noncompetitive radioimmunological binding assay. At the same dilution used in immunocytochemistry, two different NIADDK antihuman prolactin antisera displayed 49% and 24% binding of labeled rat LH beta. Similar cross reactions were demonstrated immunocytochemically. There was no cross reactivity between rat LH beta and the antibody to rat prolactin. Consequently, the staining reported to be in lactotrops in the previous study was probably in gonadotrops.

Angiotensin II↗
PubMed2003

Pituitary hormones inhibit the function and differentiation of fetal Sertoli cells.

Although the role of pituitary hormones in fetal Sertoli cell proliferation is well understood, their involvement in fetal Sertoli cell differentiation is poorly documented. In this study, we evaluated rat fetal Sertoli cell function by measuring basal transferrin secretion ex vivo and transferrin and anti-Müllerian hormone (AMH) mRNA levels in vivo. The differentiation state of the Sertoli cells was estimated from the amount of transferrin secreted ex vivo after acute stimulation with FSH. Surprisingly, we found that the amount of transferrin secreted by each Sertoli cell in basal condition and after acute FSH stimulation decreased between 18.5 and 21.5 day post coitum (dpc), which corresponds to the onset of pituitary hormone secretion. All of the Sertoli cell parameters measured (basal and FSH-stimulated transferrin secretion ex vivo, transferrin and AMH mRNA levels in vivo) were higher in 21.5-dpc fetuses that had been decapitated on 16.5 dpc than in control littermates. Furthermore, immunostaining for AMH was strongly increased after decapitation. Taken together, these results suggest that pituitary hormones in the fetus and in the immature or adult rat differently regulate Sertoli cells, which suggests that fetal Sertoli cells have their own particular physiology.

Animals↗
PubMed1985

Biochemical transmethylation of lipids and neuropeptidergic stimulation of pituitary hormone secretion.

S-adenosyl-L-methionine-dependent methylation of membrane phosphatidylethanolamine to phosphatidylcholine has been shown to exist in a number of tissues including pituitary gland and to play important roles in receptor-mediated functions. The possible role of this phospholipid methylation reaction in pituitary hormone secretion has been studied. To this end, the ability of thyrotropin-releasing hormone (TRH) to release thyrotropin (TSH) and prolactin and the ability of luteinizing hormone-releasing hormone (LH-RH) to release luteinizing hormone (LH) were evaluated after inhibition of pituitary phospholipid methylation. Both TRH and LH-RH stimulated the release of their corresponding pituitary hormone in a dose-dependent manner and this stimulatory effect was inhibited in the presence of phospholipid methylation inhibitors. Non-specific stimulation of TSH release by 55 mM KCl or 0.1 mM veratridine, however, was not affected by the methylation inhibitors. The data suggest that phospholipid methylation may participate in receptor-mediated release of pituitary hormones.

Animals↗
PubMed1996

A study of anterior pituitary hormones secretion in patients with glioma receiving interferon-beta treatment.

Human interferon beta (IFN-beta) has been used for the treatment of patients with benign and malignant astrocytomas. The effect of IFN-beta on pituitary function, however, has not been precisely evaluated before. In this study the serum levels of various anterior pituitary hormones including GH, PRL, ACTH, and TSH were measured to determine the effects of IFN-beta on pituitary endocrine function in 19 consecutive glioma patients receiving IFN-beta. Daily doses of 3 x 10(6) U of IFN-beta were administered as a 30-min intravenous drip infusion beginning at 0800 h every morning during the first week and then 4 times a week for additional 6 weeks. Blood samples were taken on the day prior to administration as controls (0900 h and 1500 h), and on the first day of administration (0900 h and 1500 h) and after 7 days of administration (0900 h) in order to determine the acute and chronic or integrated effects of IFN-beta on the above pituitary hormones. No significant change in serum concentrations of any of the pituitary hormones examined was observed, suggesting that human natural IFN-beta used for the treatment of gliomas has no significant effect on the secretion of these hormones from the pituitary in these patients.

Adolescent↗
PubMed1987

Choice of extraction procedure for estimation of anterior pituitary hormone content.

Searching for the best procedure for simultaneous estimation of the anterior pituitary hormones, extraction efficiencies of various media, additives such as urea and triton X-100, and physical treatments such as freezing-thawing (F-T) and sonication, were examined by measuring prolactin (PRL), growth hormone (GH), lutropin (LH), follitropin (FSH), and thyrotropin (TSH) in the extracts. Ethanolic media (60% EtOH) gave high yields of PRL at neutral to alkaline pH, but poor extraction of GH accompanied by a marked loss of its immunoreactivity during storage. Ethanolic media also gave a poor yield of LH even at high pH. Aqueous media like PBS at various pH, 0.1 M acetic acid and distilled water were considerably effective in the extraction of GH, LH, FSH and TSH if they were coupled with F-T and sonication. However, high yields of PRL could not be obtained with these aqueous media even with F-T and sonication. Hartree's 40% EtOH-6% ammonium acetate, pH 5.1, solubilized considerable amounts of glycoprotein hormones, but yielded almost no GH and only a small amount of PRL. The addition of triton X-100 to PBS (pH 7) at 0.1% resulted in the maximum extraction of glycoprotein hormones with homogenization and F-T, but further sonication was necessary for GH and PRL. When the anterior pituitaries were homogenized and frozen-thawed in PBS (pH 7) containing 1 M urea, yields of PRL, GH, LH, FSH, and TSH were maximum, and sonication did not cause any additional extraction, indicating that this procedure, i.e. homogenization and F-T in 1 M urea-PBS, would be the best for the simultaneous estimation of these anterior pituitary hormones.

Acetates↗
PubMed2005

The role of leptin in the regulation of pituitary hormones release.

OBJECTIVE: It has been reported that leptin plays an important role in the regulation of food intake and energy expenditure. There are controversial opinions about effects of leptin on the hormonal system. The aim of this study was to estimate the effect of leptin on pituitary hormones release after central and peripheral administration. METHODS: Leptin was injected intracerebroventricularly (icv) in a dose of 0.5 microg/5microl aCSF (artificial cerebrospinal fluid) for 5 min in Wistar Kyoto rats. At 60 and 120 min after injections the animals were decapitated. Leptin in a dose of 10 microg in 300 microl of saline was administered intravenously (i.v). At 60 mins the animals were decapitated. Serum rLH, rFSH, rPRL, rTSH, rGH concentrations were measured with RIA methods. RESULTS: After central (icv) injection of leptin we observed an increase of rGH, rTSH and a decrease of rPRL. However, after peripheral (iv) injection of leptin we found a decrease of rGH and rTSH and an increase of rPRL. We did not find any significant changes in LH and FSH after icv and iv injection of leptin. CONCLUSIONS: The opposite effects of leptin on pituitary hormones release were observed due to the method of leptin administration. Leptin may play a modulating role in the mechanism of pituitary hormones release.

Animals↗
PubMed1990

Cytokine modulation of pituitary hormone secretion.

A rapidly expanding body of evidence indicates that cytokines do indeed regulate pituitary hormone secretion. Recent studies with cytokines in vivo and in vitro support the idea that cytokines are the principal mediators of the neuroendocrine responses previously observed in infectious and inflammatory states. The dominant route of this modulation appears to be via the brain and hypothalamus, although a role for direct effects on the pituitary has not been excluded. These effects may be mediated by circulating cytokines, endogenously produced cytokines, or both. A number of receptor systems and second messengers may be involved, and a role for arachidonate metabolite pathways appears particularly likely. A final question: Of what use to the organism is the ability of immune activation to control pituitary hormone secretion? For some pituitary secretions there is a reasonable basis for speculation. Glucocorticoids serve to limit the severity of immune responses and recent studies argue that defects in this pathway permit the expression of autoimmune disease. Inhibition of thyroid function may limit the catabolic side effects of infectious illness. Stimulation of growth hormone could have the same effect, and growth hormone and prolactin may serve to enhance some immune responses.

Animals↗
PubMed1982

The effects of neurotensin on anterior pituitary hormone secretion.

The present experiments were conducted to determine the effects of neurotensin on secretion of a variety of anterior pituitary hormones. Conscious rats with indwelling cannulae in the third ventricle and external jugular vein were used and the effects on plasma hormone levels measured by radioimmunoassay. Neurotensin was found to decrease plasma prolactin levels in ovariectomized females, normal males, and males in which prolactin levels had been elevated by ether or by a combination of fluoxetine and 5-hydroxytryptaphane. The prolactin-lowering effect was blocked by alpha-methyl-tyrosine to inhibit catecholamine synthesis and by the specific dopamine receptor blocker, spiroperidol. In ovariectomized females, neurotensin was also capable of suppressing LH and elevating growth hormone following its intraventricular injection. Intravenous injection of the peptide elevated prolactin but had no effect on the release of the other pituitary hormones. When hemipituitaries of ovariectomized rats were incubated in vitro, neurotensin elevated prolactin and TSH release into the medium. The minimal effective dose to elevate prolactin and TSH release was 50 ng/ml. Release of gonadotropins and growth hormone was unaffected. It is concluded that neurotensin inhibits prolactin release by a CNS, presumably hypothalamic action, to stimulate the tuberoinfundibular dopaminergic neurons. The dopamine released then inhibits prolactin release either by a direct action on the pituitary or by release of another prolactin-inhibiting factor. In addition, the peptide has a direct prolactin-releasing action on the pituitary. Neurotensin can inhibit LH and stimulate growth hormone presumably by a hypothalamic action since there was no effect on the release of these pituitary hormones by glands incubated in vitro. Although the peptide had no effect on TSH release following its intraventricular injection, it stimulated prolactin release by pituitaries incubated in vitro. The physiological significance of these results is not yet established; however, the presence of the peptide in regions concerned with pituitary control suggests that it may play a physiological role.

5-Hydroxytryptophan↗
PubMed1976

Delayed pituitary hormone response to LRF and TRF in patients with anorexia nervosa and with secondary amenorrhea associated with simple weight loss.

The qualitative and quantitative responses of LRF-induced LH and FSH release and TRF-induced TSH and Prolactin (PRL) release were evaluated in 21 patients with anorexia nervosa, 19 patients with secondary amenorrhea associated with simple weight loss (SWL) who did not fulfill the psychologic criteria for anorexia nervosa, and 7 normal women in the early follicular phase of the menstrual cycle. Basal plasma LH and FSH were significantly lower in the anorexia nervosa group compared to the SWL group and normals (P less than 0.05). The LRF-induced integrated LH responses, however, were the same in the 3 groups and the integrated FSH responses were greater in the underweight groups when compared to normal. The time of the peak LH response (mean+/-SE) was signifantly delayed (P less than 0.01) in both the anorexia nervosa (49 +/- 6.1 min) and SWL (28 +/- 2.5 min) groups when compared to normal (17 +/- 2.3 min). The time of the FSH response was significantly delayed (P less than 0.05) in anorexia nervosa (95 +/- 9.6 min) when compared to normals (35 +/0 7.9 min) and SWL patients (62 +/- 11.7 min). Normal basal TSH and PRL and normal peak TSH and PRL responses to TRF were found in anorexia nervosa. The time of the TSH and PRL peak (56+/-8.9 and 36+/-3.6 min,, respectively) in anorexia nervosa was significantly later than normal (26 +/- 1.7 and 36 +/- 3.6 min respectively) (P less than 0.01). It is concluded that despite normal quantitative response to releasing hormones, there are abnormally delayed responses in both anorexia nervosa and SWL patients. The SWL responses were intermediate between those of the anorexia nervosa group and normals. The constellation of normal quantitative but abnormal kinetic LRF and TRF responses supports the hypothesis that the endocrine changes seen in anorexia nervosa are consistent with hypothalamic dysfunction.

Adolescent↗
PubMed1994

Pituitary hormones as neurotrophic signals: anomalous hypophysiotrophic neuron differentiation in hypopituitary dwarf mice.

Anterior pituitary hormones are known to exert dynamic negative feedback effects on their respective regulatory ("hypophysiotropic") neurons in the hypothalamus. The purpose of this review is to present the evidence for a theory that the effect of pituitary hormones on these hypophysiotropic neurons is neurotrophic, extending beyond dynamic feedback to influence upon cell survival, phenotypic differentiation, and axonal connectivity. To that end, the adult condition and the development of hypophysiotropic neurons in mutant mice which lack pituitary growth hormone (GH) and prolactin (PRL) are presented as models of the effect of absent specific neurotrophic signals. The expression of the neurohormones which inhibit PRL and GH secretion, dopamine (DA) and somatostatin, respectively, is markedly reduced in the hypothalamus of the hypopituitary dwarf mouse, and this adult condition is the result of postnatal failure to develop or actual regression, which may include neuronal cell death. The deficit in DA may be reversed by PRL replacement, but only if initiated at an identified critical postnatal period. Conversely, expression of the stimulatory GH-releasing hormone (GHRH) is markedly increased in the dwarf mouse hypothalamus. The loss of DA and the increase in GHRH occur in the same hypothalamic area, suggesting neuronal phenotypic plasticity in response to absence of pituitary feedback signals. The axonal terminations of extant GH- and PRL-regulating neurons in external median eminence appear to be reduced, suggesting that pituitary signals are required for appropriate axonal guidance during development, even though an endocrine vascular route intervenes between these regulatory neurons and their target secretory cells. The collective observations indicate that GH and PRL may be regarded as neurotrophic factors for their respective regulatory neurons in the hypothalamus.

Animals↗
PubMed1981

Opiate receptors and anterior pituitary hormone secretion in man. Effect of naloxone infusion.

The role of endogenous opioid receptors on anterior pituitary hormone secretion was evaluated by the administration of the opioid receptor antagonist naloxone. The infusion of naloxone (8 mg iv followed by 4mg/h for 3 h) did not alter basal growth hormone (GH), prolactin (Prl) and thyrotrophin (TSH) secretion but produced a significant rise in cortisol and gonadotrophins in normal man. The infusion of the opiate antagonist appeared to increase the rate and amplitude of luteinizing hormone (LH) pulsatility. Naloxone pre-medication (10 mg iv 30 min before testing) did not alter the pituitary response to TRH and LRH stimulation. These results demonstrate that naloxone can modify basal anterior pituitary hormone secretion and strongly suggest an endogenous opioid modulation of some of these hormones.

Adult↗
PubMed2000

Galanin coexists with pituitary hormones in the fetal rat.

Immunocytochemical analysis of endocrine cells of the developing rat pituitary has shown clearly that, starting from E16, the galanin-immunoreactive cells are heterogeneous, the neuropeptide being present in cells containing the majority of pituitary hormones. A proportion of galanin-containing corticotropes, starting from about 17% at E16 reached about 29% at E21, while the galanin-containing lactotrope increase in the same period was from about 13% to 34%. Galanin-containing thyrotropes ranged from about 11% at E16 to about 13% at E21, while the proportion of galanin-containing luteotropes increased consistently from about 17% at E19 to about 27% at E21. Only the trend of galanin-containing somatotropes was inverted, falling from about 26% to 13%. We conclude that the multiple coexistence of galanin with most of the pituitary hormones during fetal development is a further example of plasticity of endocrine pituitary cells, and that galanin may have a role in cytodifferentiation.

Adrenocorticotropic Hormone↗
PubMed1984

[Pituitary hormone responses to exercise at high altitudes].

The secretory responses of the anterior pituitary hormone to physiological stress were studied in healthy male volunteers. Measurements of blood LH, FSH, Prolactin, GH, ACTH, lactate, pyruvate and hematocrit were made from blood samples taken at rest, after 15 minutes at sea level, and at an altitude of 4000 m and 5500 m modulated in a climate-controlled room. The results are summarized as follows: Blood levels of Prolactin and ACTH were increased after exercise at a high altitude. Blood levels of LH and FSH after exercise at each altitude were not significantly different from those at rest. Blood GH level was increased after exercise at any altitude. Blood levels of lactate and pyruvate were increased after exercise at any altitude. These results suggest that the secretory response of the anterior pituitary hormone to physiological stress is prominent in Prolactin, GH and ACTH but not in FSH and LH.

Adrenocorticotropic Hormone↗
PubMed1997

Unchanged response to stimulation of pituitary hormone release after serial UV irradiation in men.

A group of 24 healthy young men were evaluated before and after serial suberythematous ultraviolet (UV) radiation: group I, control (no irradiation); groups II and III, 12 radiations in 4 weeks with two different spectra (both containing UV-B). Before the first and 2 days after the last exposure all the volunteers were given an intravenous injection of thyrotropin releasing hormone (TRH, protirelin 0.2 mg) and luteinizing hormone releasing hormone (LH-RH, gonadorelin 0.1 mg). The serum concentrations of TSH, follicle stimulating hormone, LH and prolactin were measured at 0, 20, 30, 45 and 60 min by radioimmunoassay. Neither basal nor stimulated levels of the pituitary hormones showed significant changes after UV radiation. The results showed that exposure to suberythematous doses of UV did not influence the regulation of pituitary hormones in these healthy individuals.

Adult↗
PubMed2003

Cellular determination in the anterior pituitary gland: PIT-1 and PROP-1 mutations as causes of human combined pituitary hormone deficiency.

In the anterior pituitary gland, five distinct hormone producing cell types are generated from common epithelial progenitor cells. This process of cellular determination is controlled by signaling molecules acting on transcription factors, which in turn regulate genes critical for the appearance of hormone producing cells. Two pituitary specific transcription factors, Pit-1 and Prop-1, which are required for generation of hormone producing cells in the anterior pituitary gland, have proved to be important in the cause of hypopituitarism in humans. Mutations in the human PIT-1 gene lead to a combined pituitary hormone deficiency characterized by lack of GH, PRL and TSH. Mutations in the PROP-1 gene, which are a more common cause of hypopituitarism, lead to a clinical phenotype characterized by GH, PRL, TSH, LH and FSH deficiency, and sometimes ACTH deficiency as well.

DNA-Binding Proteins↗