In-vitro evidence for the autoregulation of prolactin secretion at the level of the pituitary gland in the rat

1987 ◽  
Vol 115 (1) ◽  
pp. 13-18 ◽  
Author(s):  
A. M. Bentley ◽  
M. Wallis
Keyword(s):  
Monoamine Oxidase ◽  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Prolactin Secretion ◽  
Anterior Pituitary Gland ◽  
Physiological Significance ◽  
Secretory Product ◽  
Secretory Products ◽  
Male Tissue

ABSTRACT The autoregulation of rat prolactin secretion at the level of the pituitary gland was investigated, using a static incubation system. The rate of prolactin secretion from the female anterior pituitary gland in vitro was found to be constant when the medium was changed at 20-min intervals. However, when the medium was left unchanged and secretory products were allowed to accumulate, prolactin secretion began to decline within 60 min. This effect was not observed with the male tissue, where the level of accumulated prolactin did not reach that at which the inhibition occurred using female tissue. The nature of the putative secretory product causing the inhibition of prolactin secretion was investigated. Exogenous bovine prolactin (1–4 mg/l) caused an inhibition of endogenous rat prolactin secretion. Inclusion of monoamine oxidase in unchanged medium, to prevent dopamine accumulation in the medium (a possible consequence of co-storage and cosecretion with prolactin granules), did not prevent the inhibition observed in the control incubation. We therefore conclude that in-vitro autoregulation of prolactin secretion can occur at the level of the pituitary gland, probably due to the accumulated prolactin having a feedback action on the lactotroph. This might be of physiological significance if localized concentrations of the hormone within the gland are high. J. Endocr. (1987) 115, 13–18

scholarly journals Intermedin/Adrenomedullin-2 Inhibits Growth Hormone Release from Cultured, Primary Anterior Pituitary Cells

Endocrinology ◽  
2006 ◽  
Vol 147 (2) ◽  
pp. 859-864 ◽  
Author(s):  
Meghan M. Taylor ◽  
Sara L. Bagley ◽  
Willis K. Samson
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Hormone Secretion ◽  
Prolactin Secretion ◽  
Anterior Pituitary Gland ◽  
Male Rats ◽  
Pituitary Cells ◽  
Anterior Pituitary Cells ◽  
Peptide Family

Intermedin (IMD), a novel member of the adrenomedullin (AM), calcitonin gene-related peptide (CGRP), amylin (AMY) peptide family, has been reported to act promiscuously at all the known receptors for these peptides. Like AM and CGRP, IMD acts in the circulation to decrease blood pressure and in the brain to inhibit food intake, effects that could be explained by activation of the known CGRP, AM, or AMY receptors. Because AM, CGRP, and AMY have been reported to affect hormone secretion from the anterior pituitary gland, we examined the effects of IMD on GH, ACTH, and prolactin secretion from dispersed anterior pituitary cells harvested from adult male rats. IMD, in log molar concentrations ranging from 1.0 pm to 100 nm, failed to significantly alter basal release of the three hormones. Similarly, IMD failed to significantly alter CRH-stimulated ACTH or TRH-stimulated prolactin secretion in vitro. However, IMD concentration-dependently inhibited GHRH-stimulated GH release from these cell cultures. The effects of IMD, although requiring higher concentrations, were as efficacious as those of somatostatin and, like somatostatin, may be mediated, at least in part, by decreasing cAMP accumulation. These actions of IMD were not shared by other members of the AM-CGRP-AMY family of peptides, suggesting the presence of a novel, unique IMD receptor in the anterior pituitary gland and a potential neuroendocrine action of IMD to interact with the hypothalamic mechanisms controlling growth and metabolism.

Prolactin secretion and dopamine receptors of the MtTW15 transplantable pituitary tumour

1982 ◽  
Vol 94 (3) ◽  
pp. 347-NP ◽  
Author(s):  
M. J. Cronin ◽  
D. A. Keefer ◽  
C. A. Valdenegro ◽  
L. G. Dabney ◽  
R. M. MacLeod
Keyword(s):  
Pituitary Gland ◽  
Dopamine Receptors ◽  
Anterior Pituitary ◽  
Pituitary Tumour ◽  
Prolactin Secretion ◽  
Tumour Cells ◽  
Dopamine Antagonist ◽  
Cell Column ◽  
Prolactin Release

The MtTW15 transplantable pituitary tumour grown in rats was tested in vitro for the ability of dopamine agonists to affect prolactin secretion and for the existence of dopamine receptors. Prolactin release from enzymatically dispersed cells and non-enzymatically treated tissue fragments of both the tumour and the anterior pituitary gland was determined in a cell perifusion column apparatus. Dopamine (0·1–5 μmol/l), bromocriptine (50 nmol/l) and the dopamine antagonist haloperidol (100 nmol/l) had no effect on prolactin release from the tumour cells. In contrast, dopamine (500 nmol/l) inhibited prolactin secretion from normal anterior pituitary cells in a parallel cell column and haloperidol blocked this inhibition. Although oestrogen treatment in vivo stimulated prolactin release in vitro when the tumour was removed and studied in the cell column, oestrogen had no effect on the inability of dopamine to modify the prolactin secretion. Growth hormone release from the tumour cells was not affected by dopamine. Although MtTW15 cells were refractory to dopaminergic inhibition of prolactin release, the dopamine receptors present in tumour homogenates were indistinguishable from the dopamine receptors previously defined in the normal anterior pituitary gland. The binding of the dopamine antagonist [3H]spiperone to the tumour was saturable (110 fmol/mg protein), of high affinity to one apparent class of sites (dissociation constant = 0·12 nmol/l), reversible and sensitive to guanine nucleotides. The pharmacology of the binding was defined in competition studies with a large number of agonists and antagonists. From the order of potency of these agents, a dopaminergic interaction was apparent. We conclude that the prolactin-secreting MtTW15 tumour cells appear to be completely unresponsive to dopamine or to the potent dopamine agonist bromocriptine, in spite of apparently normal dopamine receptors in the tumour.

Effect of hypothalamic neuropeptides on corticotrophin release from quarters of rat anterior pituitary gland in vitro

1984 ◽  
Vol 100 (2) ◽  
pp. 219-226 ◽  
Author(s):  
S. A. Nicholson ◽  
T. E. Adrian ◽  
B. Gillham ◽  
M. T. Jones ◽  
S. R. Bloom
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Low Dose ◽  
Physiological Role ◽  
Anterior Pituitary Gland ◽  
High Concentration ◽  
Response Curves ◽  
Corticotrophin Releasing Factor ◽  
Basal Release

ABSTRACT The effect of six hypothalamic peptides on the basal release of ACTH and that induced by arginine vasopressin (AVP) or by ovine corticotrophin releasing factor (oCRF) from fragments of the rat anterior pituitary gland incubated in vitro was investigated. Dose–response curves to AVP and to oCRF were obtained, and the response to a low dose of oCRF was potentiated by a low dose of AVP. Basal release of ACTH was not affected by any of the peptides in concentrations in the range 10−12 to 10−6 mol/l, and only substance P (SP) and somatostatin (SRIF) inhibited significantly the response to oCRF in a dose-related manner. The responses to a range of doses of oCRF or AVP were reduced by 10−8 and 10 − 6 mol SP or SRIF/1, and to a greater extent by the higher dose. Except in the case of 10−6 mol SRIF/1 on the response to AVP, the response was not further diminished by preincubation of the tissue with the peptide before the stimulating agent was added. The inhibition of the responses to AVP or oCRF by 10−9 mol SP/1 was not potentiated by its combination with either 5 × 10−10 or 10−8 mol SRIF/1; the inhibitory effects were merely additive. The results suggest that although SRIF and SP are able to modulate the release of ACTH from the anterior pituitary gland, they do so only at a high concentration. In the case of SRIF these concentrations are several orders of magnitude higher than those reported to be present in the hypophysial portal blood and therefore a physiological role for this peptide in the control of ACTH secretion is unlikely. J. Endocr. (1984) 100, 219–226

scholarly journals Intercellular communication in the rat anterior pituitary gland: an in vivo and in vitro study

1975 ◽  
Vol 67 (2) ◽  
pp. 469-476 ◽  
Author(s):  
WH Fletcher ◽  
NC Anderson ◽  
JW Everett
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Hormone Secretion ◽  
In Vitro Study ◽  
Anterior Pituitary Gland ◽  
Stimulus Secretion Coupling ◽  
Unpublished Observation ◽  
Cellular Ca

The concept of "stimulus-secretion coupling" suggested by Douglas and co-workers to explain the events related to monamine discharge by the adrenal medulla (5, 7) may be applied to other endocrine tissues, such as adrenal cortex (36), pancreatic islets (4), and magnocellular hypothalamic neurons (6), which exhibit a similar ion-dependent process of hormone elaboration. In addition, they share another feature, that of joining neighbor cells via membrane junctions (12, 26, and Fletcher, unpublished observation). Given this, and the reports that hormone secretion by the pars distalis also involves a secretagogue-induced decrease in membrane bioelectric potential accompanied by a rise in cellular [Ca++] (27, 34, 41), it was appropriate to test the possibility that cells of the anterior pituitary gland are united by junctions.

scholarly journals In Vivo and In Vitro Arsenic Exposition Induces Oxidative Stress in Anterior Pituitary Gland

2016 ◽  
Vol 35 (4) ◽  
pp. 463-475 ◽  
Author(s):  
Sonia A. Ronchetti ◽  
María S. Bianchi ◽  
Beatriz H. Duvilanski ◽  
Jimena P. Cabilla
Keyword(s):  
Oxidative Stress ◽  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Inorganic Arsenic ◽  
Anterior Pituitary Gland ◽  
Pituitary Cells ◽  
Prolactin Release ◽  
Stress Responsive Genes

Inorganic arsenic (iAs) is at the top of toxic metalloids. Inorganic arsenic-contaminated water consumption is one of the greatest environmental health threats worldwide. Human iAs exposure has been associated with cancers of several organs, neurological disorders, and reproductive problems. Nevertheless, there are no reports describing how iAs affects the anterior pituitary gland. The aim of this study was to investigate the mechanisms involved in iAs-mediated anterior pituitary toxicity both in vivo and in vitro. We showed that iAs administration (from 5 to 100 ppm) to male rats through drinking water increased messenger RNA expression of several oxidative stress-responsive genes in the anterior pituitary gland. Serum prolactin levels diminished, whereas luteinizing hormone (LH) levels were only affected at the higher dose tested. In anterior pituitary cells in culture, 25 µmol/L iAs significantly decreased prolactin release in a time-dependent fashion, whereas LH levels remained unaltered. Cell viability was significantly reduced mainly by apoptosis evidenced by morphological and phosphatidylserine externalization studies. This process is characterized by early depolarization of mitochondrial membrane potential and increased levels of reactive oxygen species. Expression of some key oxidative stress-responsive genes, such as heme oxygenase-1 and metallothionein-1, was also stimulated by iAs exposure. The antioxidant N-acetyl cysteine prevented iAs-induced effects on the expression of oxidative stress markers, prolactin release, and apoptosis. In summary, the present work demonstrates for the first time that iAs reduces prolactin release both in vivo and in vitro and induces apoptosis in anterior pituitary cells, possibly resulting from imbalanced cellular redox status.

Degradation of Insulin-I131 by an Extract of Anterior Pituitary Gland

1958 ◽  
Vol 193 (3) ◽  
pp. 476-478 ◽  
Author(s):  
H. T. Narahara ◽  
R. H. Williams
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Trichloroacetic Acid ◽  
Electrophoretic Analysis ◽  
Anterior Pituitary Gland ◽  
Radioactive Material ◽  
Incubation Mixture ◽  
Pituitary Extract ◽  
Insulin Molecule

When insulin-I131 was incubated at 37°C and pH 7.5 with an extract of beef anterior pituitary, the radioactive material was rendered more soluble in trichloroacetic acid (TCA). Electrophoretic analysis of the TCA-soluble reaction product revealed that it was not free iodide. The concept that pituitary extract might contain a system capable of attacking the insulin molecule was strengthened by the observation that the addition of nonlabeled insulin to the incubation mixture decreased the rate of degradation of insulin-I131. The degradative system of beef anterior pituitary extract was found to be nondialyzable and heat-labile. The degradation of insulin by pituitary extracts may help to explain the observation of other workers that such extracts can inactivate insulin in vitro.

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