High concentrations of immunoreactive inhibin in the plasma of mares and fetal gonads during the second half of pregnancy

1996 ◽  
Vol 8 (8) ◽  
pp. 1137 ◽  
Author(s):  
Y Nambo ◽  
S Nagata ◽  
M Oikawa ◽  
T Yoshihara ◽  
N Tsunoda ◽  
...  
Keyword(s):  
Immunohistochemical Staining ◽  
Follicle Stimulating Hormone ◽  
Plasma Concentrations ◽  
Peripheral Circulation ◽  
Pituitary Cells ◽  
Rat Pituitary ◽  
High Concentrations ◽  
Rat Pituitary Cells ◽  
First Time

Plasma concentrations of immunoreactive (ir)-inhibin were measured in seven pregnant mares from around Day 140 of gestation to Day 2 after parturition using a heterologous bovine-based radioimmunoassay (RIA). Concentrations of luteinizing hormone (LH), follicle-stimulating hormone (FSH), oestradiol-17 beta, progesterone and relaxin were also measured in the same samples. A marked increase in plasma concentrations of ir-inhibin, FSH and LH occurred between Day 220 and Day 300 of gestation but the concentrations of all three hormones returned to baseline by about Day 320 (three weeks before parturition). In contrast, circulating concentrations of the three placental hormones, oestradiol-17 beta, progesterone and relaxin, increased during the final weeks of pregnancy and then decreased markedly to basal values within two days of parturition. There was a positive correlation between circulating concentrations of ir-inhibin and FSH (r = 0.75, P < 0.01) rather than the expected negative correlation. ir-inhibin was not detected in homogenates obtained at Day 190 of pregnancy and form term placenta, but high concentrations of ir-inhibin were present in homogenates of fetal and newborn gonads. Despite the high concentrations of ir-inhibin in these homogenates, they failed to exert any suppressive bioactivity on FSH secretion by rat pituitary cells cultured in vitro. Furthermore, immunohistochemical staining revealed the presence of inhibin in the interstitial cells of equine fetal gonads at Day 190 of gestation. These findings demonstrate for the first time that high concentrations of ir-inhibin, LH and FSH are secreted into the peripheral circulation of the mare during the second half of pregnancy. However, ir-inhibin present in the plasma of pregnant mares appears to be biologically inactive. This hormone is not presumed to be of placental origin but it is proposed that either the enlarged fetal gonads or the maternal ovaries, or both of these organs, may be a source of inhibin in response to the coincident increase in circulating concentrations of LH and FSH.

Inhibitory effect of the uterus on plasma and pituitary FSH in rats

1990 ◽  
Vol 124 (2) ◽  
pp. 183-189 ◽  
Author(s):  
J. C. Biro ◽  
P. Eneroth
Keyword(s):  
Molecular Weight ◽  
Chromatographic Analysis ◽  
Plasma Concentrations ◽  
Inhibitory Effect ◽  
Inhibitory Response ◽  
Pituitary Cells ◽  
Pregnant Rats ◽  
Rat Pituitary ◽  
Rat Pituitary Cells

ABSTRACT Plasma concentrations of FSH and LH were measured in ovariectomized, ovohysterectomized, hysterectomized and sham-operated adult, non-pregnant rats at 3, 14, 21 and 28 days after operation. From day 21 after the operation onwards, there were higher concentrations of FSH in plasma in ovohysterectomized than in ovariectomized animals. The concentration of LH was not influenced by hysterectomy. The inhibitory response of FSH and LH to a single dose of oestradiol was not altered by any of the operations. By 2 weeks after surgery, pituitary FSH content had increased in ovohysterectomized animals compared with ovariectomized ones, but this difference was eliminated when ovohysterectomized animals were treated with crude uterine extract. Pituitary contents of LH and prolactin were not influenced by hysterectomy or by treatment with uterine extract, thus indicating the specificity of an inhibitory effect of the uterus on FSH levels. Treatment of hysterectomized and intact animals with uterine extract resulted in a reduction in the weight of the ovaries of 23–38% (P<0·05), indirectly showing the presence of an FSH-inhibiting substance in the extract. Fractionated uterine extract inhibited FSH synthesis by rat pituitary cells in vitro, but had no effect on LH synthesis. Chromatographic analysis indicated that the FSH-inhibiting substance in the uterus has a molecular weight of 10 000–20 000. Journal of Endocrinology (1990) 124, 183–189

Modulation of prolactin secretion by contraceptive progestins in cultured rat pituitary cells in vitro

1988 ◽  
Vol 117 (4_Suppl) ◽  
pp. S188-S189
Author(s):  
L. KIESEL ◽  
T. RABE ◽  
D. SCHOLZ ◽  
V. KIRSCHNER ◽  
B. RUNNEBAUM
Keyword(s):  
Prolactin Secretion ◽  
Pituitary Cells ◽  
Rat Pituitary ◽  
Rat Pituitary Cells

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.

In vitro evidence of a role for inhibin in female rabbits

1984 ◽  
Vol 246 (3) ◽  
pp. E243-E248
Author(s):  
A. L. Goodman
Keyword(s):  
Granulosa Cells ◽  
Pituitary Cells ◽  
Dependent Manner ◽  
C Cells ◽  
Rat Pituitary ◽  
Reference Preparation ◽  
Lh Release ◽  
Rat Pituitary Cells ◽  
I Cells

To examine a regulatory role for inhibin in female rabbits, an in vitro bioassay for inhibin activity was modified to use cultured rabbit pituitary cells and charcoal-extracted porcine follicular fluid (pFFx) as a reference preparation. pFFx inhibited follicle-stimulating hormone (FSH) release in a dose-dependent manner in cultures from both intact (I) and castrate (C) does at doses that also inhibited FSH release by cultured rat pituitary cells. Basal FSH release by I cells was inhibited greater than 10% by 0.02% (vol/vol) and greater than 90% by greater than or equal to 0.2% pFFx, whereas in C cells maximal inhibition of FSH release plateaued at only approximately 75%. FSH secretion was restored after removal of pFFx in day 2 media. Luteinizing hormone (LH) release by C cells was not inhibited at any dose of pFFx, but in I cells LH was progressively inhibited to approximately 60% of control levels during day 2 (but not day 1). Charcoal-extracted media (0.25-1%) in which 5 X 10(5) rabbit granulosa cells had been earlier cultured for 72 h produced a parallel inhibition of FSH release. The present findings demonstrate that 1) rabbit pituitary cells are responsive to inhibin, i.e., pFFx preferentially inhibited FSH secretion in a direct, graded, and reversible manner and 2) rabbit follicular granulosa cells secrete an inhibin-like substance.

Induction by Tumor Necrosis Factor-Alpha of Rapid Release of Immunoreactive and Bioactive Luteinizing Hormone from Rat Pituitary Cells in vitro

1990 ◽  
Vol 52 (5) ◽  
pp. 468-472 ◽  
Author(s):  
Masaaki Yamaguchi ◽  
Masahiro Sakata ◽  
Noboru Matsuzaki ◽  
Koji Koike ◽  
Akira Miyake ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Pituitary Cells ◽  
Necrosis Factor Alpha ◽  
Rapid Release ◽  
Rat Pituitary ◽  
Factor Alpha ◽  
Rat Pituitary Cells ◽  
Necrosis Factor

Subcellular localization of Apaf-1 in apoptotic rat pituitary cells

2006 ◽  
Vol 290 (3) ◽  
pp. C672-C677 ◽  
Author(s):  
Maja Potokar ◽  
Marko Kreft ◽  
Helena H. Chowdhury ◽  
Nina Vardjan ◽  
Robert Zorec
Keyword(s):  
Cytochrome C ◽  
Single Cells ◽  
Cellular Level ◽  
Pituitary Cells ◽  
Apoptotic Pathway ◽  
Proliferation And Apoptosis ◽  
Rat Pituitary ◽  
Before And After ◽  
Rat Pituitary Cells ◽  
First Time

A key step in the intrinsic apoptotic pathway is the assembly of the apoptosome complex. The apoptosome components are well known; however, the physiology of the assembly of the apoptosome complex at the cellular level is still poorly defined. The aim of this work was to study the subcellular distribution of the apoptosome scaffold protein apoptotic protease-activating factor 1 (Apaf-1) before and after triggering apoptosis in single somatotrophs. Somatotrophs are the subject of extensive pituitary tissue remodeling in different physiological situations in which the quality and the number of pituitary cells are determined by cell proliferation and apoptosis. We show herein that 2 h after triggering apoptosis with rotenone, Apaf-1 redistributed to the proximity of mitochondria. In addition, the degree of colocalization between Apaf-1 and fluorescently labeled caspase-9 significantly increased during the same period. Furthermore, we show herein for the first time in single cells that the colocalization between Apaf-1 and cytochrome c increases only transiently, indicating a transient interaction between cytochrome c and Apaf-1 during the activation of apoptosis in these cells.

Progesterone together with estradiol promotes luteinizing hormone β-subunit mRNA stability in rat pituitary cells cultured in vitro

1996 ◽  
Vol 134 (2) ◽  
pp. 236-242 ◽  
Author(s):  
Deokbae Park ◽  
Minseok cheon ◽  
Changmee Kim ◽  
Kyungjin Kim ◽  
Kyungza Ryu
Keyword(s):  
Mrna Stability ◽  
Actinomycin D ◽  
Pituitary Cells ◽  
Mrna Levels ◽  
Ovarian Steroids ◽  
Subunit Mrna ◽  
Rat Pituitary ◽  
Lh Release ◽  
Rat Pituitary Cells

Park D, Cheon M, Kim C, Kim K, Ryu K. Progesterone together with estradiol promotes luteinizing hormoneβ-subunit mRNA stability in rat pituitary cells in vitro. Eur J Endocrinol 1996;134:236–42. ISSN 0804–4643 The present study examined the role of ovarian steroids, estradiol and/or progesterone in the regulation of luteinizing hormone β-subunit (LH-β) mRNA levels and LH release in the rat anterior pituitary cells cultured in vitro. When estradiol (10 nmol/l and/or progesterone (100 nmol/l) were added to the cultures, neither estradiol or progesterone nor both together altered the basal LH-β mRNA levels or LH release. Continuous exposure to gonadotropin-releasing hormone (GnRH, 0.2 nmol/l) for 24 h markedly induced LH-β mRNA accumulation, and in this experimental condition, progesterone alone and progesterone + estradiol further augmented GnRH-induced LH-β mRNA levels and LH release. Then we explored further the possibility that ovarian steroids are involved in modulating LH-β mRNA stability in cultured rat pituitary cells where transcription was inhibited by actinomycin D. Anterior pituitary cells were preincubated with GnRH (0.2 nmol/l) for 16 h and, after removing GnRH from culture medium, the cells were incubated further in the presence of actinomycin D (5 μmol/l) for 24 h. The LH-β mRNA levels gradually declined to about 30% of the control values (zero time point after GnRH removal) in a time-dependent manner. During this period, either progesterone alone or progesterone + estradiol clearly blocked the degradation of LH-β mRNA species. These results indicate that ovarian steroids promote LH-β mRNA stability, thereby contributing to the maintenance of GnRH-stimulated LH-β mRNA levels. Kyungza Ryu, Department of Pharmacology, College of Medicine, Yonsei University, 120-749, Seoul, Korea

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