Differential regulation of gonadotropins and glycoprotein hormone α-subunit by IGF-I in anterior pituitary cells from male rats

2004 ◽  
Vol 27 (7) ◽  
pp. 670-675 ◽  
Author(s):  
F. Pazos ◽  
F. Sánchez-Franco ◽  
J. Balsa ◽  
J. Escalada ◽  
L. Cacicedo
Keyword(s):  
Anterior Pituitary ◽  
Differential Regulation ◽  
Male Rats ◽  
Pituitary Cells ◽  
Glycoprotein Hormone ◽  
Α Subunit ◽  
Anterior Pituitary Cells ◽  
Igf I

The effects of insulin-like growth factor-I (IGF-I), IGF-II and des(1–3)IGF-I, a potent IGF analogue, on growth hormone and IGF-binding protein secretion from cultured rat anterior pituitary cells

1991 ◽  
Vol 130 (1) ◽  
pp. 93-99 ◽  
Author(s):  
J. M. Simes ◽  
J. C. Wallace ◽  
P. E. Walton
Keyword(s):  
Growth Factor ◽  
Anterior Pituitary ◽  
Pituitary Cells ◽  
Gh Secretion ◽  
Factor I ◽  
Anterior Pituitary Cells ◽  
Low Concentrations ◽  
Igf I ◽  
Igf Binding ◽  
Igf Binding Protein

ABSTRACT The effects of insulin-like growth factor-I (IGF-I), IGF-II and des(1–3)IGF-I, a potent IGF-I analogue, on the secretion of GH and IGF-binding protein (IGFBP) from cultured rat anterior pituitary cells were measured. IGF-I and des(1–3)IGF-I stimulated GH secretion at low concentrations (maximally effective at 1 and 0·1 μg/l respectively) and inhibited GH secretion at higher concentrations. The half-maximal inhibitory concentrations (IC50) were approximately 20 μg/l and 1 μg/l for IGF-I and des(1–3)IGF-I respectively. Thus des(1–3)IGF-I was more potent than IGF-I in these effects on GH secretion. We postulate that the increased potency of des(1–3)IGF-I in affecting GH secretion is due to decreased binding of this peptide by pituitary IGFBP compared with IGF-I. In contrast with IGF-I and des(1–3)IGF-I, IGF-II did not stimulate GH secretion at low concentrations, but did inhibit GH secretion from pituitary cells with an IC50 of approximately 20 μg/l. Several IGFBPs ranging in molecular mass from 22 000 to 52 000 were detected in medium conditioned by cultured anterior pituitary cells. When measured by Western-ligand blotting and competitive ligand-binding techniques, these IGFBPs exhibited decreased binding of des(1–3)IGF-I compared with IGF-I and IGF-II. The production of IGFBP by anterior pituitary cells was stimulated by the addition of IGFs to the culture medium. Journal of Endocrinology (1991) 130, 93–99

Bradykinin stimulates phosphoinositide metabolism and prolactin secretion in rat anterior pituitary cells

1989 ◽  
Vol 2 (1) ◽  
pp. 47-53 ◽  
Author(s):  
T.H. Jones ◽  
B. L. Brown ◽  
P. R. M. Dobson
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Inositol Phosphate ◽  
Prolactin Secretion ◽  
Male Rats ◽  
Pituitary Cells ◽  
Phosphoinositide Metabolism ◽  
Phosphate Accumulation ◽  
Anterior Pituitary Cells ◽  
Inositol Phosphate Accumulation

ABSTRACT Bradykinin stimulated prolactin secretion from monolayer cultures of rat anterior pituitary cells, the stimulation being greater from the cells of male rats. This stimulated secretion was accompanied by a rise in total inositol phosphate accumulation, suggesting that the action of bradykinin is mediated by phosphoinositide hydrolysis. The increase in inositol phosphate accumulation was biphasic; a further sharp rise occurred when the concentration of bradykinin exceeded 1 μmol/l. This may indicate that bradykinin acts on other cell types in the pituitary gland. Bradykinin had no effect on growth hormone secretion from cells of normal pituitary glands, or on prolactin secretion and phosphoinositide metabolism in GH3 rat pituitary tumour cells. Bradykinin receptor antagonists (both B1 and B2) had no effect on either bradykinin-stimulated inositol phosphate accumulation or prolactin secretion. Kallikreins, the enzymes responsible for the generation of kinins, are known to be present in the adenohypophysis. Therefore, the results presented here would suggest that kinins may have a role as paracrine agents in the pituitary gland.

Blockade by lithium ions of potassium channels in rat anterior pituitary cells

1991 ◽  
Vol 261 (2) ◽  
pp. C218-C223 ◽  
Author(s):  
M. Kato ◽  
P. M. Lledo ◽  
J. D. Vincent
Keyword(s):  
Growth Hormone ◽  
Anterior Pituitary ◽  
Hormone Secretion ◽  
Male Rats ◽  
Delayed Rectifier ◽  
Pituitary Cells ◽  
Patch Clamp Technique ◽  
Anterior Pituitary Cells ◽  
K Current ◽  
K Currents

Extracellular Li+ has been known to facilitate the basal secretion of growth hormone from anterior pituitary cells and of catecholamine from chromaffin cells. In both cases, the intracellular accumulation of Li+ seems to be the prerequisite, and the presence of extracellular Ca2+ is indispensable. In this series of experiments, we examined whether Li+ blocked K+ currents by using primary cultured anterior pituitary cells from male rats. K+ currents were measured in the whole cell configuration of the patch-clamp technique. Extracellular Li+ (140 mM) suppressed both the delayed rectifier K+ current (IK) and the transient outward K+ current to 71 and 69% of control, respectively, in a reversible manner. IK elicited by a voltage step to +70 mV from holding potential of -70 mV was suppressed by 32.5 mM internal Li+ to 28% of control. Half-maximal suppression of K+ conductance by internal Li+ was 16 mM. Furthermore, Ca(2+)-channel blocker methoxyverapamil potently suppressed Li(+)-induced growth hormone secretion. From these results we propose that the blockade by Li+ of K+ channels could depolarize the cells and activate Ca2+ channels, thereby promoting the influx of Ca2+ and hormone secretion as a mechanism of Li(+)-induced hormone secretion.

scholarly journals Characterization of the Mechanism of Inhibin α-Subunit Gene in Mouse Anterior Pituitary Cells by RNA Interference

PLoS ONE ◽  
2013 ◽  
Vol 8 (10) ◽  
pp. e74596 ◽  
Author(s):  
Li Han ◽  
Canjie Wu ◽  
Hasan Riaz ◽  
Liya Bai ◽  
Jianguo Chen ◽  
...  
Keyword(s):  
Rna Interference ◽  
Anterior Pituitary ◽  
Pituitary Cells ◽  
Subunit Gene ◽  
Α Subunit ◽  
Anterior Pituitary Cells

Insulin, insulin-like growth factor I (IGF-I) and IGF-II enhance basal and gonadotrophin-releasing hormone-stimulated luteinizing hormone release from rat anterior pituitary cells in vitro

1994 ◽  
Vol 131 (6) ◽  
pp. 641-645 ◽  
Author(s):  
Renza Soldani ◽  
Angelo Cagnacci ◽  
Samuel SC Yen
Keyword(s):  
Growth Factor ◽  
Anterior Pituitary ◽  
Pituitary Cells ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Anterior Pituitary Cells ◽  
Igf I ◽  
Lh Release ◽  
Growth Factor I

Soldani R, Cagnacci A, Yen SSC. Insulin, insulin-like growth factor I (IGF-I) and IGF-II enhance basal and gonadotrophin-releasing hormone-stimulated luteinizing hormone release from rat anterior pituitary cells in vitro. Eur J Endocrinol 1994;131:641–5. ISSN 0804–4643 The role of insulin-like growth factor I (IGF-I) and IGF-II on luteinizing hormone (LH) release is still unclear. The present study was performed to investigate modifications of basal and gonadotrophinreleasing hormone (GnRH)-stimulated (109 mol/l) LH release, induced by a 4-h and a 24-h incubation with physiological doses of IGF-I (1, 5 and 10 nmol/l) and IGF-II (5, 10 and 15 nmol/l) in comparison with insulin (0.0017, 0.1722 and 1.722 nmol/l), from primary cultures of male rat anterior pituitary cells. Both during the 4-h and the 24-h incubation, basal and GnRH-stimulated LH release were increased by IGF-I, IGF-II and insulin in a dose-dependent fashion. Present data confirm insulin's capability of potentiating anterior pituitary LH release from dispersed rat anterior pituitary cells in vitro, and reveal similar effects for physiological doses of IGF-I and IGF-II. Renza Soldani, Instituto di Ginecologia Ostetricia e Fisiopatologia della Riproduzione Umana, Ospedale S. Giovanni di Dio, via Ospedale 46, 09124 Cagliari, Italy

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.

Responsiveness of chicken embryonic somatotropes to somatostatin (SRIF) and IGF-I

1997 ◽  
Vol 154 (2) ◽  
pp. 303-310 ◽  
Author(s):  
M M Piper ◽  
T E Porter
Keyword(s):  
Embryonic Development ◽  
Anterior Pituitary ◽  
Pituitary Cells ◽  
Gh Secretion ◽  
Anterior Pituitary Cells ◽  
Igf I

Abstract We have previously demonstrated that chicken embryonic somatotropes are responsive to GHRH shortly after they differentiate. In contrast, relatively little is known about the regulation of GH secretion by somatostatin (SRIF) and IGF-I during chicken embryonic development. In the present study, anterior pituitary cells were isolated from day 16, 18 and 20 embryos and subjected to reverse hemolytic plaque assays (RHPAs) for chicken GH to assess the effect of SRIF and IGF-I on basal GH release and SRIF on GHRH-stimulated GH secretion. We found that all three ages responded to SRIF, under both basal and stimulated conditions. SRIF inhibition of basal GH release was evident for day 18 and 20 cells by 9 h, while 18 h were required for day 16 cells. After 18 h, 10−11 m SRIF depressed basal GH secretion by day 16 and 18 cells, while 10−9 m SRIF was required to depress GH plaque percentages by day 20 cells. GHRH stimulated GH release from all ages tested. After 2 h, SRIF partially suppressed GHRH-stimulated GH release by day 20 cells. After 6 h, day 18 cells responded to SRIF, reducing the percentage of plaque-forming cells under GHRH stimulated conditions. After 18 h, the percentage of day 16 cells forming GH plaques was reduced for cells treated with GHRH and SRIF, compared with cells treated with GHRH alone. All ages examined also responded to IGF-I. After 36 h, GH release by day 16 and 18 cells was decreased when exposed to IGF-I. While IGF-I decreased the relative amount of GH secreted per somatotrope on day 20, a paradoxical increase in the percentage of cells secreting GH was noted. These results indicate that anterior pituitary somatotropes are responsive to SRIF and IGF-I during late embryonic development of chickens. Journal of Endocrinology (1997) 154, 303–310

scholarly journals The hormonal status modulates the effect of neurokinin A on prolactin secretion in female rats

1998 ◽  
Vol 159 (3) ◽  
pp. 389-395 ◽  
Author(s):  
D Pisera ◽  
S Theas ◽  
A De Laurentiis ◽  
M Lasaga ◽  
B Duvilanski ◽  
...  
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
In Vitro Release ◽  
Anterior Pituitary Gland ◽  
Female Rats ◽  
Male Rats ◽  
Neurokinin A ◽  
Pituitary Cells ◽  
Anterior Pituitary Cells ◽  
Ovx Rats

We have previously reported that neurokinin A (NKA), a tachykinin closely related to substance P, increases the release of prolactin (PRL) from the anterior pituitary gland of male rats, but not from pituitaries of ovariectomized (OVX) female rats. In this study, we evaluated the influence of estrogens in the action of NKA on PRL secretion in female rats. NKA stimulated the in vitro release of PRL from pituitary glands of OVX-chronically estrogenized rats, and of proestrus and estrus rats, but had no effect in anterior pituitaries of diestrus rats. In addition, we observed that cultured anterior pituitary cells of OVX rats responded to NKA only when they were incubated for 3 days in the presence of estradiol 10(-9) M. This effect was blocked by L-659,877, an NK-2 receptor antagonist. We also studied the action of NKA on PRL release during lactation. The response of anterior pituitary cells to NKA was variable over this period. The maximal sensitivity to NKA was observed at day 10 of lactation. Furthermore, the blockade of endogenous NKA by the administration of an anti-NKA serum to lactating rats reduced the PRL surge induced by the suckling stimulus. These results show that the responsiveness of the anterior pituitary gland of female rats to NKA is modulated by the endocrine environment, and suggest that NKA may participate in the control of PRL secretion during the estrus cycle and lactation.

Sign in / Sign up

Export Citation Format

Share Document