Inhibition by extracellular Na+ replacement of GRF-induced GH secretion from rat pituitary cells

1988 ◽  
Vol 254 (4) ◽  
pp. E476-E481 ◽  
Author(s):  
M. Kato ◽  
M. A. Hattori ◽  
M. Suzuki
Keyword(s):  
Anterior Pituitary ◽  
Channel Blocker ◽  
Na Channel ◽  
Pituitary Cells ◽  
Ionic Mechanism ◽  
Camp Production ◽  
Normal Medium ◽  
Gh Secretion ◽  
Rat Pituitary ◽  
Rat Pituitary Cells

To further clarify the ionic mechanism of the action of growth hormone (GH)-releasing factor (hGRF) on GH secretion, the involvement of extracellular Na+ was studied in perifused dispersed rat anterior pituitary cells. Replacing extracellular Na+ with mannitol or tris(hydroxymethyl)aminomethane (Tris+) suppressed hGRF- and dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP)-induced GH secretion. The peak responses to a 2-min application of 1 nM hGRF were 165.0 +/- 5.6 ng/ml (normal medium, mean +/- SE), 21.2 +/- 1.4 ng/ml (Na+-free, mannitol medium), and 18.0 +/- 1.7 ng/ml (Na+-free, Tris+ medium). GH secretion induced by DBcAMP was also suppressed by Na+ replacement to less than 50% of that in normal medium. However, either 15 or 30 mM KCl-stimulated GH secretion was not markedly affected by replacement of Na+ with either compound. Tetrodotoxin, a voltage-sensitive Na+ channel blocker, had no effect on either hGRF- or excess K+-induced GH secretion. cAMP production by hGRF was not greatly affected by replacing extracellular Na+. Thus extracellular Na+ plays an important role in hGRF-induced GH secretion, especially in the process after cAMP production. The involvement of cAMP-sensitive Na+ channels in hGRF-stimulated GH secretion is discussed.

Involvement of thioredoxin in the regulation of growth hormone secretion in rat pituitary cell cultures

2001 ◽  
Vol 281 (2) ◽  
pp. E269-E274 ◽  
Author(s):  
Ikue Hata ◽  
Yosuke Shigematsu ◽  
Yusei Ohshima ◽  
Hirokazu Tsukahara ◽  
Kazuo Fujisawa ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Anterior Pituitary ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Pituitary Cells ◽  
Dependent Manner ◽  
Gh Secretion ◽  
Anterior Pituitary Cells ◽  
Rat Pituitary ◽  
Rat Pituitary Cells

We report here an examination of the effect of thioredoxin (TRX) on the secretion of growth hormone (GH) from rat anterior pituitary cells in vitro. Treatment of rat pituitary cells with growth hormone-releasing factor (GRF), but not GH, led to a significant increase in intracellular TRX protein levels. GRF, recombinant human TRX (rhTRX), and a combination thereof were all shown to induce immediate GH secretion from pituitary cells, as evidenced by perifusion experiments. RhTRX, but not other reducing agents such as β-mercaptoethanol and N-acetyl-l-cysteine, augmented GRF-stimulated and -unstimulated GH secretion from rat pituitary cells in a dose-dependent manner. RhTRX did not significantly affect the GH mRNA expression of pituitary cells stimulated in the presence or absence of GRF. In addition, rhTRX-augmented GH secretion was not significantly affected by the presence of cycloheximide. Collectively, these findings suggest that TRX is induced by stimulation with GRF and plays a regulatory role in GH secretion from rat anterior pituitary cells by enhancing the secretion of stored GH, rather than by the synthesis of GH.

scholarly journals CircAgtpbp1 Acts as a Molecular Sponge of miR-543-5p to Regulate the Secretion of GH in Rat Pituitary Cells

Animals ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 558
Author(s):  
ZeWen Yu ◽  
WenZhi Ren ◽  
Tian Wang ◽  
WeiDi Zhang ◽  
ChangJiang Wang ◽  
...  
Keyword(s):  
Pituitary Gland ◽  
Inhibitory Effect ◽  
Pituitary Cells ◽  
Sequencing Analysis ◽  
Hormone Regulation ◽  
Gh Secretion ◽  
Qrt Pcr ◽  
Rat Pituitary ◽  
Rat Pituitary Cells

CircRNAs have been identified to be expressed differently and stably in numerous species and tissues, but their functions in growth hormone (GH) secretion are still largely unknown. In summary, we have revealed a circRNA-miRNA-mRNA network that may play a biological role in the rat pituitary gland. First, we verified the chromosome location information of circAgtpbp1 according to sequencing analysis. The circAgtpbp1 characteristics were authenticated through PCR, qRT–PCR, treating with RNase and fluorescent in situ hybridization (FISH). Second, we detected the expression pattern of circAgtpbp1 in the rat anterior pituitary by qRT–PCR. We also designed circAgtpbp1 siRNA and constructed overexpression plasmid to evaluate the effect of circAgtpbp1 function on GH secretion by qRT–PCR, ELISA and Western blot. CircAgtpbp1 is a stable, truly circular molecule. We found that circAgtpbp1 interacted with miR-543-5p and can regulate GH secretion in pituitary cells through a circAgtpbp1-miR-543-5p-GH axis. Overall, the evidence generated by our study suggests that circAgtpbp1 can act as a sponge of miR-543-5p to reduce the inhibitory effect of miR-543-5p on Gh1 and further promote GH secretion. These findings expand our existing knowledge on the mechanisms of hormone regulation in the pituitary gland.

A COMPARISON OF THE EFFECTS OF FOUR ERGOT DERIVATIVES ON PROLACTIN SECRETION BY DISPERSED RAT PITUITARY CELLS

1980 ◽  
Vol 87 (1) ◽  
pp. 95-103 ◽  
Author(s):  
G. DELITALA ◽  
T. YEO ◽  
ASHLEY GROSSMAN ◽  
N. R. HATHWAY ◽  
G. M. BESSER
Keyword(s):  
Anterior Pituitary ◽  
Ergot Alkaloids ◽  
Prolactin Secretion ◽  
Pituitary Cells ◽  
Inhibitory Effects ◽  
Prolactin Release ◽  
Ergot Derivatives ◽  
Rat Pituitary ◽  
Rat Pituitary Cells

The inhibitory effects of dopamine and various ergot alkaloids on prolactin secretion were studied using continuously perfused columns of dispersed rat anterior pituitary cells. Bromocriptine (5 nmol/l) and lisuride hydrogen maleate (5 nmol/l) both inhibited prolactin secretion, the effects persisting for more than 3 h after the end of the administration of the drugs. A similar although less long-lasting effect was observed with lergotrile (50 nmol/l) and the new ergoline derivative, pergolide (5 nmol/l). These effects contrasted with the rapid disappearance of the action of dopamine. The potency estimates of the ergots relative to that of dopamine were: lergotrile, 2·3; bromocriptine, 13; lisuride, 15; pergolide, 23. The dopamine-receptor blocking drugs, metoclopramide and haloperidol, antagonized the prolactin release-inhibiting activity of the compounds; bromocriptine and lisuride showed the highest resistance to this dopaminergic blockade. The results suggested that the direct effect of the ergot derivatives on dispersed pituitary cells was mediated through dopamine receptors and emphasized the long-lasting action of bromocriptine and lisuride in vitro.

PACAP 38 regulates prolactin (PRL) and growth hormone (GH) secretion and gene expression in cultured rat pituitary cells

1992 ◽  
Vol 40 (2) ◽  
pp. 289
Author(s):  
L. Zheng ◽  
M. Kazemzadeh ◽  
B. Velkeniers ◽  
A. Vandermeers ◽  
J. Christophe ◽  
...  
Keyword(s):  
Gene Expression ◽  
Growth Hormone ◽  
Pituitary Cells ◽  
Gh Secretion ◽  
Rat Pituitary ◽  
Rat Pituitary Cells

scholarly journals Corticotropin-Releasing Factor (CRF) Agonists Stimulate Testosterone Production in Mouse Leydig Cells through CRF Receptor-1*

Endocrinology ◽  
1998 ◽  
Vol 139 (2) ◽  
pp. 651-658 ◽  
Author(s):  
Nadja Heinrich ◽  
Mike R. Meyer ◽  
Jens Furkert ◽  
Annette Sasse ◽  
Michael Beyermann ◽  
...  
Keyword(s):  
Leydig Cell ◽  
Leydig Cells ◽  
Pituitary Cells ◽  
Camp Production ◽  
Cos Cells ◽  
Testosterone Production ◽  
Primary Mouse ◽  
Rat Pituitary ◽  
Rat Pituitary Cells ◽  
Mouse Leydig Cell

Abstract The influence of CRF on testosterone production in primary mouse Leydig cell cultures was studied, and the type of CRF receptor (CRF-R) involved in this activity was determined. CRF directly stimulated testosterone production in mouse Leydig cells, but did not influence the maximum human (h)CG-induced testosterone production. The effect was time- and dose-dependent, saturable with an EC50 of 2.84 nm for hCRF, antagonized by the CRF antagonist α-helical CRF9–41, and accompanied by intracellular cAMP elevation. The rank order of potency of the natural CRF agonists, hCRF, ovine CRF, sauvagine, and urotensin, corresponded to that of their activities on CRF-R1 in rat pituitary cells and also to that reported for this receptor, but not for CRF-R2, when transfected into various cell lines. Furthermore, the difference in response of mouse Leydig cells to[ 11-d-Thr,12-d-Phe]- and[ 13-d-His,14-d-Leu]-ovine CRF corresponded to that measured when COS cells expressing CRF-R1 were activated, but was considerably smaller than that observed for activation of COS cells expressing CRF-R2α or -R2β. The messenger RNA encoding the mouse CRF-R1 was detected by RT-PCR in mouse Leydig cell preparations. In contrast to mouse Leydig cells, CRF agonists had no influence on the basal testosterone and cAMP production by rat Leydig cells, nor did the agonists or antagonist change the hCG-stimulated testosterone and cAMP production by these cells. It is concluded that mouse Leydig cells express CRF-R1, mediating elevation of testosterone production by CRF agonists through cAMP. Because potencies of CRF agonists in activating mouse Leydig cells were more than 10-fold lower compared with their potencies in stimulating rat pituitary cells, it is suggested that the coupling of the CRF-R1 to intracellular signaling in Leydig cells is different from that in corticotropic pituitary cells, at least in quantitative terms.

scholarly journals Is GHRH Receptor Essential to GHRP-2-Induced GH Secretion in Primary Cultured Rat Pituitary Cells?

Endocrinology ◽  
2002 ◽  
Vol 143 (5) ◽  
pp. 1964-1967 ◽  
Author(s):  
Sang-Gun Roh ◽  
Chen Chen ◽  
Ki-Choon Choi ◽  
Yogendra Shrestha ◽  
Shin-Ichi Sasaki
Keyword(s):  
Pituitary Cells ◽  
Gh Secretion ◽  
Ghrh Receptor ◽  
Rat Pituitary ◽  
Rat Pituitary Cells

scholarly journals GH secretion by cultured rat pituitary cells under radiotherapy

1981 ◽  
Vol 15 (12) ◽  
pp. 1570-1570
Author(s):  
Z Hochberg ◽  
A Kuten ◽  
P Hertz ◽  
A Benderli
Keyword(s):  
Pituitary Cells ◽  
Gh Secretion ◽  
Rat Pituitary ◽  
Rat Pituitary Cells
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