Inhibition by testosterone of prolactin and growth hormone release from chicken anterior pituitary glands in vitro

1984 ◽  
Vol 102 (2) ◽  
pp. 153-159 ◽  
Author(s):  
T. R. Hall ◽  
S. Harvey ◽  
A. Chadwick
Keyword(s):  
Anterior Pituitary ◽  
Prolactin Secretion ◽  
Prostaglandin E ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Prolactin Release ◽  
Thyrotrophin Releasing Hormone ◽  
Pituitary Glands ◽  
Stimulation Of

ABSTRACT Pituitary glands and hypothalami from broiler fowl were incubated in medium containing testosterone, and prolactin and GH release were determined. Pituitary glands were also preincubated for 20 h in medium containing testosterone, and then in medium containing various secretagogues. Testosterone inhibited the release of prolactin directly from the pituitary gland in a concentration-related manner. The hypothalamus stimulated the release of prolactin, but by a lesser amount in the presence of testosterone. When pituitary glands were preincubated with testosterone, subsequent release of prolactin was inhibited, except with the highest concentration which stimulated prolactin release. Hypothalamic extract (HE) markedly stimulated prolactin release from control pituitary glands although testosterone-primed glands were less responsive. The stimulation of prolactin release by thyrotrophin releasing hormone (TRH) and prostaglandin E2 (PGE2) was also reduced by preincubation of the pituitary glands with testosterone. Priming with testosterone did not affect the release of GH from pituitary glands alone, but reduced the TRH-, HE- and PGE2-stimulated release of GH. These results demonstrate that testosterone directly inhibits prolactin secretion and reduces the sensitivity of pituitary lactotrophs and somatotrophs to provocative stimuli. J. Endocr. (1984) 102, 153–159

The dopaminergic regulation of anterior pituitary 45Ca2+ homeostasis and prolactin secretion

1986 ◽  
Vol 108 (3) ◽  
pp. 423-429 ◽  
Author(s):  
M. P. Schrey ◽  
H. J. Clark ◽  
S. Franks
Keyword(s):  
Dopamine Agonist ◽  
Anterior Pituitary ◽  
Prolactin Secretion ◽  
Prolactin Release ◽  
Pituitary Glands ◽  
Dopaminergic Regulation ◽  
Cellular Ca ◽  
Stimulation Of ◽  
Dopaminergic Control

ABSTRACT A role for the regulation of cellular Ca2+ homeostasis in the dopaminergic control of prolactin secretion was investigated in rat anterior pituitary glands. Withdrawal of dopamine stimulated the uptake of 45Ca2+ into hemipituitary tissue by 48% after 3 min. Radioisotope desaturation from tissue prelabelled with 45Ca2+ was significantly retarded in the presence of dopamine. Withdrawal of dopamine rapidly stimulated 45Ca2+ efflux from prelabelled tissue by 79% and was accompanied by a three- to fourfold rise in prolactin secretion. The 45Ca2+ efflux response to dopamine withdrawal was reduced in tissue prelabelled in the presence of dopamine. Agonist displacement with metoclopramide mimicked the effect of dopamine withdrawal on 45Ca2+ efflux and prolactin secretion. These observations demonstrate that the stimulation of prolactin release by dopamine withdrawal is accompanied by a redistribution of cellular Ca2+ and support the hypothesis that dopamine inhibits secretion by decreasing Ca2+ influx in the mammotroph cell. J. Endocr. (1986) 108, 423–429

Age-related changes in prolactin and growth hormone release from pituitary glands in vitro

1985 ◽  
Vol 108 (4) ◽  
pp. 479-484 ◽  
Author(s):  
T. R. Hall ◽  
S. Harvey ◽  
A. Chadwick
Keyword(s):  
Growth Hormone ◽  
Anterior Pituitary ◽  
Hormone Secretion ◽  
Age Groups ◽  
The Other ◽  
Hormone Release ◽  
Thyrotrophin Releasing Hormone ◽  
Age Related ◽  
Pituitary Glands

Abstract. The basal release of prolactin from cockerel anterior pituitary glands in vitro declined between 1 and 7 weeks of age, to a level less than that released by pituitary glands from 18 week old (adult) cockerels and hens. Basal growth hormone (GH) release increased between 1 and 7 weeks of age but had declined in adults to a level similar to that released from 4 weeks old cockerels. The responsiveness of the pituitary gland to hypothalamic stimulation, using hypothalami from 8 week old broiler fowl, was also age-related. Prolactin release was considerably higher from pituitaries of 1 week old cockerels compared to the other age groups. Stimulation of GH release by the hypothalamus was higher from pituitaries of both 1 and 7 week old cockerels compared to the other groups of birds. The increase in release of prolactin following incubation with thyrotrophin releasing hormone (TRH) declined between 1 and 7 weeks, but increased slightly in adult birds, whereas the increase in release of GH following TRH was higher from pituitaries of both 1 and 7 week old cockerels. Hypothalamic prolactin (Prl) releasing activity, measured as the ability of the hypothalamus to stimulate hormone release from 8 week old broiler fowl anterior pituitary glands, declined with the age of the donor cockerels. The hypothalami from adult hens secreted significantly more Prl releasing activity than did adult cockerel hypothalami. The secretion of GH releasing activity decreased markedly with the age of the donor bird. These results suggest that maturational patterns of hormone secretion in fowl are partly due to changes in autonomous hormone release, to changing patterns of hypothalamic activity and to differences in pituitary responsiveness to provocative stimuli.

Desensitization of rat anterior pituitary gland to thyrotrophin releasing hormone

1984 ◽  
Vol 101 (1) ◽  
pp. 101-105 ◽  
Author(s):  
M. C. Sheppard ◽  
K. I. J. Shennan
Keyword(s):  
Anterior Pituitary ◽  
Prolactin Secretion ◽  
Normal Medium ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Pituitary Tissue ◽  
Subsequent Response ◽  
Pituitary Glands ◽  
Prolactin Response

ABSTRACT We have studied the secretion of TSH and prolactin from perifused rat anterior pituitary glands in vitro in response to single pulses of thyrotrophin releasing hormone (TRH) and KCl after prior exposure to TRH. Anterior pituitary fragments were incubated in normal medium or in medium containing 28 nmol TRH/1 for 20 h before perifusion. Thyrotrophin releasing hormone (28 nmol/l), administered as a 3-min pulse, stimulated TSH and prolactin release from control tissue to a peak value four or five times that of basal. After exposure of the pituitary tissue to TRH for 20 h, the subsequent response of TSH to a 3-min pulse of TRH was, however, markedly reduced; in contrast, the prolactin response was not significantly reduced. In a similar series of experiments KCl (60 nmol/l) was administered to both control and TRH-'treated' pituitary tissue as a 3-min pulse; no significant differences in TSH responses or prolactin responses were observed. These data indicate that TRH desensitizes the pituitary thyrotroph to a subsequent TRH stimulus but has very little effect on prolactin secretion. J. Endocr. (1984) 101, 101–105

Dopaminergic inhibition of prolactin release from pituitary glands of the domestic fowl incubated in vitro

1984 ◽  
Vol 103 (1) ◽  
pp. 63-69 ◽  
Author(s):  
T. R. Hall ◽  
A. Chadwick
Keyword(s):  
Pituitary Gland ◽  
Prolactin Secretion ◽  
Prolactin Release ◽  
Dopaminergic Drugs ◽  
Thyrotrophin Releasing Hormone ◽  
Two Factors ◽  
Pituitary Glands ◽  
Hypothalamic Tissue ◽  
Regulation Of Secretion

ABSTRACT Anterior pituitary glands from broiler fowl were incubated by themselves, with hypothalamic tissue or with thyrotrophin releasing hormone (TRH) in medium containing dopamine and its antagonist pimozide. The presence of hypothalamic tissue or TRH resulted in a stimulation of release of prolactin. Neither dopamine nor pimozide affected prolactin release directly from the pituitary gland. Dopamine inhibited the release of prolactin stimulated by hypothalamic tissue or TRH, in a concentration-dependent fashion. Pimozide diminished the response to dopamine. After pituitary glands were preincubated for 20 h in medium containing oestradiol-17β, the basal release of prolactin was enhanced as was the response to TRH. Both basal and TRH-stimulated release of prolactin from the oestrogen-primed pituitary glands was inhibited by dopamine, an effect blocked by pimozide. Hypothalami from broiler fowl were incubated for up to 8 h in medium containing dopaminergic drugs and pituitary glands were incubated in this medium, alone or with pimozide. As indicated by the prolactin released by the pituitary glands, the hypothalami appeared to secrete prolactin-releasing activity in a time-related fashion. Dopaminergic activity was also present in the hypothalami, since pimozide enhanced the prolactin-releasing activity of the medium. Dopamine apparently inhibited and pimozide stimulated the secretion of releasing activity from the hypothalamus. These results suggest that dopamine inhibits release of prolactin directly from the pituitary gland only when prolactin secretion is high. The hypothalamus secretes at least two factors regulating prolactin secretion, a prolactin-releasing factor and a dopaminergic prolactin-inhibiting factor. Dopamine may also play an inhibitory role in the regulation of secretion of the prolactin-releasing factor. J. Endocr. (1984) 103, 63–69

NEUROTRANSMITTER EFFECTS ON RELEASE OF PROLACTIN AND GROWTH HORMONE IN VITRO FROM PITUITARY GLANDS OF THE PIGEON, COLUMBA LIVIA

1982 ◽  
Vol 92 (2) ◽  
pp. 303-308 ◽  
Author(s):  
T. R. HALL
Keyword(s):  
Growth Hormone ◽  
Pituitary Gland ◽  
Anterior Pituitary ◽  
In Vitro Release ◽  
Columba Livia ◽  
Hormone Release ◽  
Thyrotrophin Releasing Hormone ◽  
Pituitary Glands ◽  
Vitro Release

Single pigeon anterior pituitary glands were incubated with or without a hypothalamus in media containing various drugs. Release of prolactin and growth hormone was quantified by an electrophoretic-densitometric method. The hypothalamus stimulated release of both prolactin and growth hormone from the pituitary gland. Dopamine did not affect hormone release from pituitary glands incubated alone, but inhibited hypothalamus-stimulated release of prolactin and augmented hypothalamus-stimulated release of growth hormone in a dose-related manner. The effects of dopamine were reversed by its antagonist, pimozide. Serotonin stimulated release of prolactin and inhibited release of growth hormone from pituitary–hypothalamus co-incubations, and these effects were blocked by its antagonist, methysergide. Thyrotrophin releasing hormone (TRH) stimulated release of both hormones directly from pituitary glands incubated alone. Dopamine now inhibited TRH-stimulated release of prolactin, without affecting TRH-stimulated release of growth hormone. These results indicate that the neurotransmitters, dopamine and serotonin, affect the in-vitro release of factors from the hypothalamus which control the secretion of prolactin and growth hormone. In addition, dopamine may inhibit release of prolactin directly from the pituitary gland, but only when secretion of prolactin is high initially.

scholarly journals Biosynthesis of growth hormone in the rat anterior pituitary gland. Stimulation of biosynthesis in vitro by insulin

1973 ◽  
Vol 134 (4) ◽  
pp. 1103-1113 ◽  
Author(s):  
A. Betteridge ◽  
M. Wallis
Keyword(s):  
Growth Hormone ◽  
Anterior Pituitary ◽  
Rna Synthesis ◽  
Glucose Utilization ◽  
Actinomycin D ◽  
Hormone Synthesis ◽  
Pituitary Glands ◽  
Hormone Biosynthesis ◽  
Stimulation Of

The effect of insulin on the incorporation of radioactive leucine into growth hormone was investigated by using rat anterior pituitary glands incubated in vitro. A 50% stimulation over control values was observed at insulin concentrations above 2μm (280munits/ml). The effect was specific for growth hormone biosynthesis, over the range 1–5μm-insulin (140–700munits/ml). Lower more physiological concentrations had no significant effect in this system. Above 10μm (1.4 units/ml) total protein synthesis was also increased. The stimulation of growth hormone synthesis could be partially blocked by the addition of actinomycin D, suggesting that RNA synthesis was involved. Insulin was found to stimulate the rate of glucose utilization in a similar way to growth hormone synthesis. 2-Deoxyglucose and phloridzin, which both prevented insulin from stimulating glucose utilization, also prevented the effect of insulin on growth hormone synthesis. If glucose was replaced by fructose in the medium, the effect of insulin on growth hormone synthesis was decreased. We conclude that the rate of utilization of glucose may be an important step in mediating the effect of insulin on growth hormone synthesis.

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.

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.

Characterization of the somatostatin-like immunoreactivity extracted from an adrenal medullary tumour

1982 ◽  
Vol 2 (3) ◽  
pp. 147-154 ◽  
Author(s):  
R. Corder ◽  
J. E. C. Sykes ◽  
P. J. Lowry
Keyword(s):  
Growth Hormone ◽  
Anterior Pituitary ◽  
Gel Filtration ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Identical Composition ◽  
Salt Fractionation ◽  
Somatostatin 14

Significant amounts of somatostatin-like immunor reactivity (SLI) were detected in the extract of a human catecholamine-secreting adrenal medullary tumour. After salt fractionation and reconstitution the major portion of SLI was purified by gel filtration and two HPLC steps; in all three systems it eluted in the position of somatostatin-14. The purified somatostatin-like peptide inhibited, in a dose-related manner, growth hormone release from stimulated perfused rat anterior pituitary ceils in vitro. Amino acid analysis showed the purified peptide to have an identical composition to somatostatin found in other species.

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