Cellular localization of apelin and its receptor in the anterior pituitary: evidence for a direct stimulatory action of apelin on ACTH release

2007 ◽  
Vol 292 (1) ◽  
pp. E7-E15 ◽  
Author(s):  
Annabelle Reaux-Le Goazigo ◽  
Rodrigo Alvear-Perez ◽  
Philippe Zizzari ◽  
Jacques Epelbaum ◽  
Marie-Thérèse Bluet-Pajot ◽  
...  
Keyword(s):  
Anterior Pituitary ◽  
Cellular Localization ◽  
Physiological Role ◽  
Nerve Fibers ◽  
Male Rat ◽  
Stimulatory Action ◽  
Receptor Mrna ◽  
Apelin Receptor ◽  
Acth Release

Apelin is a bioactive peptide recently identified as the endogenous ligand of the human orphan G protein-coupled receptor APJ. The presence of apelin-immunoreactive nerve fibers, together with the detection of apelin receptor mRNA in the parvocellular part of the paraventricular nucleus and the stimulatory action of apelin on corticotropin-releasing hormone release, indicate that apelin modulates adrenocorticotropin (ACTH) release via an indirect action on the hypothalamus. However, a direct action of apelin in the anterior pituitary cannot be excluded. Here, we provided evidence for the existence of an apelinergic system within the adult male rat pituitary gland. Double immunofluorescence staining indicated that apelin is highly coexpressed in the anterior pituitary, mainly in corticotrophs (96.5 ± 0.3%) and to a much lower extent in somatotropes (3.2 ± 0.2%). Using in situ hybridization combined with immunohistochemistry, a high expression of apelin receptor mRNA was also found in corticotrophs, suggesting a local interaction between apelin and ACTH. In an ex vivo perifusion system of anterior pituitaries, apelin 17 (K17F, 10−6 M) significantly increased basal ACTH release by 41%, whereas apelin 10 (R10F, 10−6 M), an inactive apelin fragment, was ineffective. In addition, K17F but not R10F induced a dose-dependent increase in K+-evoked ACTH release, with maximal increase being observed for a 10−6 M concentration. Taken together, these data outline the potential role of apelin as an autocrine/paracrine-acting peptide on ACTH release and provide morphological and neuroendocrine basis for further studies that explore the physiological role of apelin in the regulation of anterior pituitary functions.

scholarly journals History and perspectives of pituitary folliculo-stellate cell research

2005 ◽  
Vol 153 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Wilfried Allaerts ◽  
Hugo Vankelecom
Keyword(s):  
Cell Population ◽  
Anterior Pituitary ◽  
Hormone Secretion ◽  
Physiological Role ◽  
Pituitary Cell ◽  
Stem Cell Population ◽  
Cell Group ◽  
Pituitary Hormone ◽  
Topographical Distribution

Historically, the study of folliculo-stellate (FS) cells of the anterior pituitary dates back to the onset of electron microscopical observation of the pituitary gland. The morphological and electrophysiological characteristics, topographical distribution and contribution to intercellular junctions of these FS cells have been instrumental to the understanding of their putative function. Moreover, many studies have documented the role of FS cells as a source of newly discovered peptides, growth factors and cytokines. Quantitative immunohistochemical observation of FS cells in situ and functional in vitro studies, using either cultured FS cells or cells from an immortalized FS cell line, forwarded the notion of immunophenotypical and functional heterogeneity of the FS cell group. Double immunolabeling with a classical FS cell marker (S-100 protein) and with major histocompatibility complex class II markers characteristic for dendritic cells (DC) have shown a considerable overlap of FS cells with DC. The latter cells are immunocompetent cells belonging to the mononuclear phagocyte system. In this review, the FS cell heterogeneity is discussed with respect to the question of their embryological origin and developmental fate and with respect to the physiological relevance of functionally heterogeneous subpopulations. Recent findings of a myeloid origin of part of the interstitial cells of the anterior pituitary are confronted by other developmental paradigms of pituitary cell differentiation. The possibility that FS cells represent an adult stem cell population of the pituitary is critically examined. Also the physiological role of FS cells in the interferon-γ- and nitric oxide-mediated effects on pituitary hormone secretion is discussed. New approaches for the study of this enigmatic cell group using immortalized cell lines and new markers for an hitherto unrecognized pituitary cell population, the so-called ‘side population’, are evaluated.

Physiological role of galanin in the regulation of anterior pituitary function in humans

1994 ◽  
Vol 266 (1) ◽  
pp. E57-E61 ◽  
Author(s):  
A. Giustina ◽  
M. Licini ◽  
M. Schettino ◽  
M. Doga ◽  
G. Pizzocolo ◽  
...  
Keyword(s):  
Anterior Pituitary ◽  
Physiological Role ◽  
Thyroid Stimulating Hormone ◽  
Pituitary Function ◽  
Slight Reduction ◽  
Baseline Serum ◽  
Releasing Hormone ◽  
Anterior Pituitary Function ◽  
Stimulating Hormone

The aim of our study was to elucidate the physiological role of the neuropeptide galanin in the regulation of anterior pituitary function in human subjects. Six healthy men (age range 26-35 yr, body mass index range 20-24 kg/m2) underwent in random order 1) an intravenous bolus injection of growth hormone-releasing hormone (GHRH)-(1-29)-NH2 (100 micrograms) + thyrotropin-releasing hormone (TRH, 200 micrograms) + luteinizing hormone-releasing hormone (LHRH, 100 micrograms) + corticotropin-releasing hormone (CRH, 100 micrograms), and 2) intravenous saline (100 ml) at time 0 plus either human galanin (500 micrograms) in saline (100 ml) or saline (100 ml) from -15 to +30 min. Human galanin determined a significant increase in serum GH (GH peak: 11.3 +/- 2.2 micrograms/l) from both baseline and placebo levels. No significant differences were observed between GH values after galanin and those after GHRH alone (24.3 +/- 5.2 micrograms/l). Human galanin significantly enhanced the GH response to GHRH (peak 49.5 +/- 10 micrograms/l) with respect to either GHRH or galanin alone. Human galanin caused a slight decrease in baseline serum adrenocorticotropic hormone (ACTH; 16.3 +/- 2.4 pg/ml) and cortisol levels (8 +/- 1.5 micrograms/dl). Galanin also determined a slight reduction in both the ACTH (peak 27 +/- 8 pg/ml) and cortisol (peak 13.8 +/- 1.3 micrograms/dl) responses to CRH. Baseline and releasing hormone-stimulated secretions of prolactin, thyroid-stimulating hormone, LH, and follicle-stimulating hormone were not altered by galanin. Our data suggest a physiological role for the neuropeptide galanin in the regulation of GH secretion in humans.(ABSTRACT TRUNCATED AT 250 WORDS)

THE DETERMINATION OF CORTICOTROPHIN-RELEASING ACTIVITY IN STEROID-BLOCKED MICE

1964 ◽  
Vol 46 (1) ◽  
pp. 71-79 ◽  
Author(s):  
Claus Rerup
Keyword(s):  
Synthetic Peptides ◽  
Anterior Pituitary ◽  
Physiological Role ◽  
Weight Basis ◽  
Corticotrophin Releasing Factor ◽  
Lysine Vasopressin ◽  
Threshold Doses ◽  
Transmitter Substance

ABSTRACT The possibility of elaborating a sensitive test for the determination of CRF (Corticotrophin-releasing factor) was investigated in corticosteroid-blocked mice. Two synthetic peptides known to possess corticotrophin-releasing activity (CRA) in the rat, i. e. lysine-vasopressin and histidyl-seryl-lysine-vasopressin (CRA-41) were used as test substances. The results showed that it is possible to perform quantitative estimations of CR-activity and that both the peptides tested are true corticotrophin-releasing substances in mice. Lysine-vasopressin was more potent than its synthetic histidyl-seryl-analogue both on an absolute weight basis and in terms of pressor- or corticotrophin equivalents. Threshold doses for CR-activity of lysine-vasopressin in mice were calculated to be about 4 ng (nanograms). From the findings it appears that in mice, the main blocking action of the glucocorticoid dexamethasone is exerted at hypothalamic or higher centres, and not in the cells of the anterior pituitary gland. It is proposed to abandon arbitrary units for CR-activity and to use vasopressin or hypothalamic extracts as a standard for CRF-assay. The possibility of a physiological role of vasopressin as a transmitter substance for corticotrophin-release is briefly discussed.

Role of the Anterior Pituitary in the Development of a Fatty Liver

1958 ◽  
Vol 193 (1) ◽  
pp. 65-68 ◽  
Author(s):  
Ira G. Wool ◽  
M. S. Goldstein
Keyword(s):  
Fatty Liver ◽  
Lipid Accumulation ◽  
Anterior Pituitary ◽  
Physiological Role ◽  
Female Rats ◽  
Hepatic Lipids ◽  
Hypophysectomized Rats

This study was undertaken to determine whether a fat mobilizing factor from the anterior pituitary is essential to the development of a fatty liver. The method employed was the administration of ethionine, an antimetabolite of methionine, to fasted female rats. Hypophysectomy led to a marked impairment in the ability to accumulate hepatic lipids. Cortisone alone or combined with thyroxine failed to restore this defect. Epinephrine administered to cortisone-maintained hypophysectomized rats led to the development of a fatty liver. While lipid accumulation in the liver can precede in the absence of a specific anterior pituitary fat mobilizing factor, the quantitative aspects do not exclude a possible physiological role for such a principle.

scholarly journals Data Supporting a New Physiological Role for Brain Apelin in the Regulation of Hypothalamic Oxytocin Neurons in Lactating Rats

Endocrinology ◽  
2011 ◽  
Vol 152 (9) ◽  
pp. 3492-3503 ◽  
Author(s):  
Laurence Bodineau ◽  
Christopher Taveau ◽  
Hong-Hanh Lê Quan Sang ◽  
Guillaume Osterstock ◽  
Isabelle Queguiner ◽  
...  
Keyword(s):  
Direct Action ◽  
Physiological Role ◽  
Double Immunofluorescence ◽  
Endogenous Ligand ◽  
Electrophysiological Measurements ◽  
Apelin Receptor ◽  
Immunofluorescence Labeling ◽  
G Protein Coupled

Apelin is a bioactive peptide identified as the endogenous ligand of the human orphan G protein-coupled receptor APJ in 1998. The present data show that apelin modulates the activity of magnocellular and parvocellular oxytocin (OXY) neurons in the lactating rat. A combination of in situ hybridization and immunohistochemistry demonstrated the presence of apelin receptor mRNA in hypothalamic OXY neurons. Double immunofluorescence labeling then revealed the colocalization of apelin with OXY in about 20% of the hypothalamic OXY-positive neurons. Intracerebroventricular apelin administration inhibited the activity of magnocellular and parvocellular OXY neurons, as shown by measuring the c-fos expression in OXY neurons or by direct electrophysiological measurements of the electrical activity of these neurons. This effect was correlated with a decrease in the amount of milk ejected. Thus, apelin inhibits the activity of OXY neurons through a direct action on apelin receptors expressed by these neurons in an autocrine and paracrine manner. In conclusion, these findings highlight the inhibitory role of apelin as an autocrine/paracrine peptide acting on OXY neurons during breastfeeding.

scholarly journals Interaction between substance P and TRH in the control of prolactin release

2000 ◽  
Vol 166 (2) ◽  
pp. 373-380 ◽  
Author(s):  
BH Duvilanski ◽  
D Pisera ◽  
A Seilicovich ◽  
M del Carmen Diaz ◽  
M Lasaga ◽  
...  
Keyword(s):  
Substance P ◽  
Anterior Pituitary ◽  
Prolactin Secretion ◽  
Male Rat ◽  
Prolactin Release ◽  
Anterior Pituitary Function ◽  
Specific Antagonist ◽  
Autocrine Factor

Substance P (SP) may participate as a paracrine and/or autocrine factor in the regulation of anterior pituitary function. This project studied the effect of TRH on SP content and release from anterior pituitary and the role of SP in TRH-induced prolactin release. TRH (10(-7) M), but not vasoactive intestinal polypeptide (VIP), increased immunoreactive-SP (ir-SP) content and release from male rat anterior pituitary in vitro. An anti-prolactin serum also increased ir-SP release and content. In order to determine whether intrapituitary SP participates in TRH-induced prolactin release, anterior pituitaries were incubated with TRH (10(-7) M) and either WIN 62,577, a specific antagonist of the NK1 receptor, or a specific anti-SP serum. Both WIN 62,577 (10(-8) and 10(-7) M) and the anti-SP serum (1:250) blocked TRH-induced prolactin release. In order to study the interaction between TRH and SP on prolactin release, anterior pituitaries were incubated with either TRH (10(-7) M) or SP, or with both peptides. SP (10(-7) and 10(-6) M) by itself stimulated prolactin release. While 10(-7) M SP did not modify the TRH effect, 10(-6) M SP reduced TRH-stimulated prolactin release. SP (10(-5) M) alone failed to stimulate prolactin release and markedly decreased TRH-induced prolactin release. The present study shows that TRH stimulates ir-SP release and increases ir-SP content in the anterior pituitary. Our data also suggest that SP may act as a modulator of TRH effect on prolactin secretion by a paracrine mechanism.

Catecholamines and pituitary function. IV. Effects of low-dose dopamine infusion and long-term bromocriptine treatment on the abnormal thyrotroph (TSH) dynamics in patients with pathological hyperprolactinaemia

1986 ◽  
Vol 111 (2) ◽  
pp. 154-161 ◽  
Author(s):  
Ildo Nicoletti ◽  
Paolo Filipponi ◽  
Leone Fedeli ◽  
Franca Ambrosi ◽  
Camillo Giammartino ◽  
...  
Keyword(s):  
Anterior Pituitary ◽  
Low Dose ◽  
Physiological Role ◽  
Serum Concentrations ◽  
Trh Test ◽  
Synthesis Inhibitor ◽  
Tsh Secretion ◽  
Insight Into

Abstract. In order to gain further insight into the role of dopamine (DA) in the control of TSH release and to investigate whether an increased or defective DA inhibition on pituitary thyrotrophs may be considered responsible for the abnormal TSH dynamics in pathological hyperprolactinaemia, we examined the effect of low-dose DA infusion on TRH stimulated TSH secretion in normally cycling women and in patients with pathological hyperprolactinaemia. The effect of long-term bromocriptine therapy on TSH dynamics was also evaluated in a selected group of hyperprolactinaemic women. Fifty-two hyperprolactinaemic patients with no other signs of pituitary or thyroid dysfunction had significantly higher mean TSH serum concentrations and mean TSH peak values after TRH administration than 75 healthy controls. Furthermore, the TSH rises induced by the DA-synthesis inhibitor α-methyl-p-tyrosine (AMPT, 500 mg orally) were enhanced in both prolactinoma and 'idiopathic hyperprolactinaemia' patients as compared with controls. There was a positive correlation between the TRH- and AMPT-induced TSH rises in the hyperprolactinaemic group. Low-dose DA infusion (0.1 μg/kg min) reduced TSH response to TRH in both regularly cycling women and patients with hyperprolactinaemic amenorrhoea. Long-term bromocriptine therapy (2.5 mg tid over 60– 150 days) not only normalized serum Prl levels, but also reduced the TSH response to TRH in 7 hyperprolactinaemic women who had presented exaggerated TSH responses to the basal TRH test. These findings confirm that DA plays a physiological role in the inhibition of TSH release, probably at the level of the anterior pituitary. The fact that both low-dose DA infusion and long-term bromocriptine treatment effectively reduced TSH release in hyperprolactinaemic patients seems to indicate that endogenous DA inhibition of pituitary thyrotrophs is reduced rather than enhanced in pathological hyperprolactinaemia.

Diurnal Variations of Plasma Growth Hormone and Brain Monoamines in Adult Male Rats

1973 ◽  
Vol 51 (12) ◽  
pp. 890-892 ◽  
Author(s):  
R. Collu ◽  
J. C. Jéquier ◽  
J. Letarte ◽  
G. Leboeuf ◽  
J. R. Ducharme
Keyword(s):  
Growth Hormone ◽  
Adult Male ◽  
Physiological Role ◽  
Male Rats ◽  
Male Rat ◽  
Plasma Growth Hormone ◽  
Gh Secretion ◽  
Adult Male Rat ◽  
Plasma Gh

Brain levels of monoamines (MA) in the adult male rat show a diurnal pattern of secretion with noradrenaline (NA) and serotonin (5-HT) reaching a peak at 1300 and 1800, respectively, and dopamine (DA) showing a bimodal pattern with peaks at 0500 and 1800. Plasma growth hormone (GH) values fluctuate widely during the nycthemeral period. Statistically significant correlations between plasma GH and brain MA levels, confirming the existence of a physiological role of MA in the control of GH secretion, could not be demonstrated in the present study.

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