DIFFERENCES IN THE RELEASE OF MELANOCYTE-STIMULATING HORMONE IN VITRO BY RAT PITUITARY GLANDS COLLECTED AT VARIOUS TIMES DURING THE OESTROUS CYCLE

1978 ◽  
Vol 78 (1) ◽  
pp. 1-6 ◽  
Author(s):  
ADRIANA VIVAS ◽  
MARÍA ESTER CELIS
Keyword(s):  
Pituitary Gland ◽  
Oestrous Cycle ◽  
Biological Assay ◽  
Melanocyte Stimulating Hormone ◽  
Pituitary Tissue ◽  
Rat Pituitary ◽  
Pituitary Glands ◽  
Stimulating Hormone

The release of melanocyte-stimulating hormone (MSH) into the medium during incubation and the pituitary tissue content of MSH were measured separately using pituitary glands collected from rats at various stages of the oestrous cycle. The MSH was measured by a biological assay using a synthetic α-MSH as standard. The release of MSH was maximal during the pro-oestrous phase and MSH content of the pituitary gland was highest during dioestrus. The influences of the tripeptide Pro-Leu-Gly-NH2, which inhibits MSH secretion in vivo, and of progesterone on the release of MSH in vitro were studied with tissue collected at various phases of the oestrous cycle. Pro-Leu-Gly-NH2 was effective in inhibiting MSH release both at pro-oestrus and oestrus but not at dioestrus. Progesterone overcame this inhibition.

RESPONSES OF RAT FETAL ADRENALS TO SYNTHETIC ADRENOCORTICOTROPHIC HORMONE AND α-MELANOCYTE-STIMULATING HORMONE: IN-VIVO AND IN-VITRO STUDIES

1982 ◽  
Vol 92 (1) ◽  
pp. 23-30 ◽  
Author(s):  
J. P. DUPOUY
Keyword(s):  
Physiological Role ◽  
Female Rats ◽  
Fetal Life ◽  
Melanocyte Stimulating Hormone ◽  
Pituitary Glands ◽  
High Doses ◽  
And Function ◽  
Stimulating Hormone

The response of the adrenals from rat fetuses at 16,18 and 20 days of gestation to 1–24 ACTH and α-melanocyte-stimulating hormone (α-MSH) was studied in vitro. The response to 1–24 ACTH increased as gestation progressed. By the end of fetal life, corticosterone release induced by ACTH from whole adrenals was greater than that observed with adrenal tissue from non-pregnant adult female rats. High doses of α-MSH also stimulated adrenal activity but the response to ACTH was always higher than that to α-MSH. The effect of 1–24 ACTH and α-MSH on fetal adrenal growth was also compared in vivo. The adrenal atrophy induced by fetal hypophysectomy on day 17 of gestation could be prevented by i.m. administration of 10 μg 1–24 ACTH or α-MSH. However, the adrenal growth was greater in ACTH-treated fetuses than in α-MSH-treated ones. Later in gestation, between days 19 and 20, 1–24 ACTH but not α-MSH was able to prevent atrophy induced by fetal hypophysectomy. These findings are discussed in relation to the literature on levels of ACTH and α-MSH in the plasma and pituitary glands of the rat throughout the last third of gestation. High levels of ACTH in the fetal circulation contrast sharply with very weak or undetectable concentrations of α-MSH. Since the present data suggest that both trophic and steroidogenic activities of ACTH were greater than those of α-MSH, it may be concluded that ACTH but not α-MSH plays a major physiological role during gestation in the regulation of both fetal adrenal growth and function in the rat.

In-vivo and in-vitro secretion of prolactin by lactating rat adenohypophyses as a function of intracellular age

1984 ◽  
Vol 101 (1) ◽  
pp. 27-32 ◽  
Author(s):  
F. Mena ◽  
G. Martínez-Escalera ◽  
C. Clapp ◽  
C. E. Grosvenor
Keyword(s):  
Pituitary Gland ◽  
Incubation Period ◽  
Gel Electrophoresis ◽  
Polyacrylamide Gel Electrophoresis ◽  
Polyacrylamide Gel ◽  
Pituitary Glands ◽  
H 26

ABSTRACT Adenohypophysial prolactin of lactating rats was pulse-labelled by [3H]leucine injected i.v. at the time of removal of the pups. The [3H]prolactin concentration in the pituitary gland, analysed by polyacrylamide-gel electrophoresis, progressively fell as the time from labelling to removal of the pituitary gland increased from 8 to 24 h, which suggests that there was a loss of hormone as it aged within the gland. Suckling effectively provoked the depletion–transformation of total and [3H]prolactin (extracted at pH 7·2) when applied after 8 h but not when applied after either 16 or 24 h after removing the pups. In rats whose pups were removed for 8 h, suckling also depleted–transformed [3H]prolactin labelled 4 h, but not that labelled 1 h before suckling. The pituitary glands of other lactating rats were labelled with [3H]leucine injected i.v. at various times before removing the glands and incubating them in medium 199. The secretion into the medium of [3H]prolactin labelled either 4, 8, 16 or 24 h beforehand was maximal during the first 30 min then declined from 30 to 240 min of incubation. However, secretion of prolactin labelled 1 h and 10 min beforehand reached a maximum after 0·5–1 h and 2 h of incubation respectively, then remained constant during the remainder of the 4-h incubation period. The total 4-h secretion of [3H]prolactin was greatest (65% of preincubation concentration) from those glands labelled 4 h before in contrast to those labelled 10 min (15%) or 1 (38%), 8 (34%), 16 (18%) or 24 h (26%) before incubation. Taken together, these data suggest that prolactin synthesized 4 h earlier is more likely to be released in response to physiological stimuli than is more recently formed prolactin or prolactin which has remained in the pituitary gland for 16 h or longer. J. Endocr. (1984) 101, 27–32

Homologous and heterologous regulation of somatostatin-binding sites on chicken adenohypophysial membranes

1990 ◽  
Vol 127 (3) ◽  
pp. 417-425 ◽  
Author(s):  
S. Harvey ◽  
J. S. Baidwan ◽  
D. Attardo
Keyword(s):  
Pituitary Gland ◽  
Binding Sites ◽  
Recombinant Dna ◽  
Inhibitory Effect ◽  
Partial Recovery ◽  
Caudal Lobe ◽  
Direct Inhibitory Effect ◽  
Pituitary Glands

ABSTRACT Binding of 125I-labelled [Tyr1]-somatostatin (125I-[Tyr1]-SRIF) to pituitary caudal lobe membranes was suppressed in immature chickens 1 and 2 h after i.v. administration of unlabelled SRIF at concentrations of 1–100 μg/kg. In-vitro preincubation of chicken pituitary glands for 0·5–4·0 h with 0·1 μmol SRIF/l similarly reduced the binding of 125I-[Tyr1]-SRIF to caudal lobe membrane preparations. After a 4-h incubation in 0·1 mmol SRIF/l, the withdrawal of SRIF from the incubation media was accompanied 4 h later by a partial recovery in the binding of 125I-[Tyr1]-SRIF to pituitary membranes. Passive immunoneutralization of endogenous SRIF resulted in a prompt (within 1 h) and sustained (for at least 24 h) suppression of 125I-[Tyr1]-SRIF binding to pituitary membranes. The i.m. administration of cysteamine (300 mg/kg) to 12-week-old birds depleted hypothalamic SRIF stores and decreased the density of 125I-[Tyr1]-SRIF-binding sites in the caudal and cephalic lobes of the chicken pituitary gland. The reduction in SRIF content and in SRIF-binding sites occurred within 1 h of cysteamine administration and was maintained for at least 24 h. In 6-week-old birds, cysteamine (300 mg/kg) administration suppressed pituitary binding of 125I-[Tyr1]-SRIF for at least 5 days. Circulati concentrations of GH were markedly decreased 1 and 4 h after cysteamine injection, but not after 24 h. Pituitary binding sites for 125I-[Tyr1]-SRIF were not affected by pretreatment of pituitary glands for 2–12 h in vitro with thyroxine or oestradiol-17β (1 nmol/l–10 μmol/l) or with ovine GH or recombinant DNA-derived chicken GH (1–100 μg/ml in vitro and 100–1000 μg/kg in vivo). Ovine prolactin, at concentrations of 1–100 μg/ml was also without effect on 125I-[Tyr1]-SRIF binding to pituitary membranes following a 2- or 4-h incubation with pituitary glands. Pituitary binding sites for 125I-[Tyr1]-SRIF were, however, increased after a 24-h incubation with 1 μmol tri-iodothyronine (T3)/l in vitro and 4 and 24 h after the administration of T3 (100–1000 μg/kg) in vivo. Although T3 had no direct inhibitory effect on 125I-[Tyr1]-SRIF binding to pituitary membranes, binding was suppressed 1 and 2 h after the in-vivo administration of T3 at concentrations of 100–1000 μg/kg. These results therefore demonstrate homologous and heterologous regulation of SRIF-binding sites in the chicken pituitary gland. Journal of Endocrinology (1990) 127, 417–425

EFFECT OF TESTOSTERONE PROPIONATE ON THE RELEASE OF FSH FROM THE PITUITARY GLAND

1968 ◽  
Vol 57 (2) ◽  
pp. 289-295 ◽  
Author(s):  
E. Steinberger ◽  
G. Duckett
Keyword(s):  
Pituitary Gland ◽  
Leydig Cell ◽  
Testosterone Propionate ◽  
Follicle Stimulating Hormone ◽  
Inhibitory Effect ◽  
Blood Levels ◽  
Rat Pituitary ◽  
Pituitary Glands ◽  
Marked Drop ◽  
Stimulating Hormone

ABSTRACT On the basis of a study of changes in follicle stimulating hormone (FSH) levels in rat pituitary glands, obtained at various times after orchiectomy, it has been previously suggested that the Leydig cell secretions may regulate the release of FSH from the pituitary gland (Steinberger & Duckett 1966). This hypothesis was put to test in the present study. FSH levels have been determined in the pituitary gland and plasma of normal, testosterone-treated, orchiectomized, and orchiectomized testosteronetreated rats. A marked drop of pituitary FSH levels, associated with an elevation of plasma FSH levels, was observed in orchiectomized rats. Administration of testosterone to orchiectomized rats prevented the drop in pituitary FSH levels and rendered the blood levels undetectable. These results are interpreted as supporting the hypothesis that testosterone has an inhibitory effect on the release of FSH from the pituitary gland.

Hypothalamic dopamine and catechol oestrogens in rats with spontaneous pituitary tumours

1983 ◽  
Vol 96 (2) ◽  
pp. 347-352 ◽  
Author(s):  
R. A. Prysor-Jones ◽  
J. J. Silverlight ◽  
J. S. Jenkins
Keyword(s):  
Pituitary Gland ◽  
Plasma Prolactin ◽  
Pituitary Tumours ◽  
Dopamine Concentration ◽  
Rat Pituitary ◽  
Pituitary Glands ◽  
Normal Rat ◽  
Old Rats ◽  
Hypothalamic Dopamine

Dopamine concentration within the hypothalamus and its depletion after the administration of α-methyl-para-tyrosine were measured in young rats and compared with values obtained in aged animals with and without spontaneously occurring pituitary tumours. Old rats had significantly reduced hypothalamic dopamine concentrations and there was less depletion of dopamine compared with young animals but there were no differences between tumorous and non-tumorous animals. Hyperprolactinaemia induced in young animals caused a much greater depletion of hypothalamic dopamine than in old tumorous rats with comparable plasma prolactin concentrations. The catechol oestrogen 2-hydroxyoestradiol inhibited the release of prolactin from normal rat pituitary glands in vitro but measurement of catechol oestrogens in the hypothalamus showed no differences between young and old tumorous or non-tumorous rats. It is concluded that reduced dopamine concentration and an impaired response to hyperprolactinaemia in old rats may facilitate the growth of prolactin-secreting tumours arising in the pituitary gland.

ETUDE DE L'ACTION DU FACTEUR HYPOTHALAMIQUE LRF (LH-RELEASING FACTOR) CHEZ LE RAT IN VIVO & IN VITRO

1967 ◽  
Vol 55 (3) ◽  
pp. 481-496 ◽  
Author(s):  
Marian Jutisz ◽  
Annette Bérault ◽  
Marie-Anne Novella ◽  
Geneviève Ribot
Keyword(s):  
Dose Response ◽  
Crude Extract ◽  
Response Curve ◽  
Assay Method ◽  
Hypothalamic Extract ◽  
Rat Pituitary ◽  
Pituitary Glands ◽  
Releasing Effect

ABSTRACT A highly purified ovine LH-releasing factor (LRF) was obtained by a modification of the method previously described. After the fractionation of a crude hypothalamic extract on a Sephadex G-25 column, the LRF fraction was desalted and partially purified by chromatography on a Dowex 50 × 12 column and on an Amberlite CG 4B column. The last step of this method, chromatography on a CMC column, gave a purification of about 1600 times with respect to the crude extract. The action of this highly purified LRF preparation was studied on rat pituitary glands in vivo and in vitro. The method used in vivo was the evaluation of the LH-releasing effect of LRF in chronically ovariectomized, steroid-blocked rats (Ramirez & McCann 1963 b). A procedure was developed which allows a 4-fold concentration of the plasma LH from these rats, so that it can be assayed by a 4-point assay method. In the in vitro method, the pituitary glands of ovariectomized steroidblocked rats (Schally & Bowers 1964 a) were incubated in a Krebs-Ringer buffer with or without LRF, and the LH released into the medium was assayed using the O.A. A.D. method of Parlow. A dose-response curve was established between the log doses of LRF and the amount of LH released. This method can be used as a sensitive and specific assay for LRF. It was shown that a dose of 1.22 μg of LRF releases approximately 5 μg of LH per mg of pituitary tissue. This is about double of the amount of this hormone originally present in the pituitary glands of these rats (2.7 μg/mg). This leads us to the conclusion that the excess of this hormone was probably synthetized during the process of incubation. The amount of steroids injected as a blocking agents, appears to be very important for both in vivo and in vitro tests.

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