Role of Arachidonate Metabolism on the in vitro Release of Luteinizing Hormone and Prolactin from the Anterior Pituitary Gland: Possible Involvement of Lipoxygenase Pathway

1986 ◽  
Vol 43 (3) ◽  
pp. 428-434 ◽  
Author(s):  
Domenico Conte ◽  
Paolo Falaschi ◽  
Antonella Proietti ◽  
Rosaria D’Urso ◽  
Franca Citarella ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Anterior Pituitary ◽  
In Vitro Release ◽  
Anterior Pituitary Gland ◽  
Lipoxygenase Pathway ◽  
Arachidonate Metabolism ◽  
Vitro Release

THE ROLE OF SEX STEROID HORMONES IN MODULATING THE RESPONSIVENESS OF THE ANTERIOR PITUITARY GLAND TO LUTEINIZING HORMONE RELEASING FACTOR IN THE FEMALE RAT

1974 ◽  
Vol 62 (3) ◽  
pp. 553-572 ◽  
Author(s):  
M. S. AIYER ◽  
G. FINK
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Anterior Pituitary Gland ◽  
Second Phase ◽  
Female Rat ◽  
Blood Samples ◽  
Sequential Administration ◽  
Oestradiol Benzoate

SUMMARY The role of ovarian hormones in the development of increased sensitivity of the anterior pituitary gland to synthetic luteinizing hormone releasing factor (LH-RF) which occurs before and during the preovulatory surge of luteinizing hormone (LH) in the rat has been examined. The response of the pituitary gland was determined, with respect to the secretion of LH and follicle-stimulating hormone (FSH), after the intravenous injection of 50 ng LH-RF/100 g body weight. The LH-RF was injected 30–60 min after the administration of sodium pentobarbitone at either 13.30 h or 18.80 h of pro-oestrus. Blood samples were collected immediately before and at frequent intervals after the injection of LH-RF, and the concentration of LH and FSH in these samples was measured by radioimmunoassay. Ovariectomy at 10.00–11.00 h of dioestrus reduced the LH response to LH-RF injected at 14.00 h of pro-oestrus, while oestradiol benzoate administered immediately after ovariectomy restored and even augmented this response. These data together with the finding that administration of the antioestrogen, ICI 46 474, at 17.00 h of dioestrus reduced the LH response to LH-RF injected on the afternoon of pro-oestrus indicates that the initial phase of increased pituitary sensitivity to LH-RF is dependent upon the marked rise in the concentration of oestradiol-17β in plasma which precedes the preovulatory surge of LH. The abrupt, marked increase in pituitary sensitivity to LH-RF, which, in the normal cycle, occurs between 14.00 and 18.30 h of pro-oestrus, failed to develop in rats ovariectomized on the morning of dioestrus whether or not oestradiol benzoate was administered after the operation. However, the LH response to LH-RF injected on the evening of pro-oestrus increased significantly when progesterone was administered at 13.00 h of pro-oestrus in rats ovariectomized and treated with oestradiol benzoate at 10.00–11.00 h of dioestrus. This suggests that the development of the second phase of increased pituitary sensitivity to LH-RF depends, at least partially, on progesterone acting on an oestrogen-primed pituitary gland. The concentrations of FSH in blood samples taken before injection of LH-RF at either 14.00 or 18.30 h of pro-oestrus were significantly greater in ovariectomized compared with those in sham-operated rats. In contrast the FSH responses, in terms of the mean maximal increments, were not significantly different in the various groups irrespective of the nature or time of operation or the time of injection of LH-RF. The FSH response to LH-RF was not appreciably altered by treatment with either oestradiol benzoate or progesterone immediately after ovariectomy although it was increased significantly by the sequential administration of oestrogen and progesterone. The significance of the findings that under certain conditions there were considerable differences between the LH and FSH responses to synthetic LH-RF is discussed with respect to the hypothesis that there is a common releasing factor for both gonadotrophins.

RELATIVE ACTIVITY, PLASMA ELIMINATION AND TISSUE DEGRADATION OF SYNTHETIC LUTEINIZING HORMONE RELEASING HORMONE AND CERTAIN OF ITS ANALOGUES

1979 ◽  
Vol 80 (1) ◽  
pp. 141-152 ◽  
Author(s):  
A. D. SWIFT ◽  
D. B. CRIGHTON
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Inverse Correlation ◽  
Anterior Pituitary Gland ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Lh Rh

The abilities of three nonapeptide analogues of synthetic luteinizing hormone releasing hormone (LH-RH) to release luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in anoestrous and cyclic ewes were examined, as were their elimination from the plasma in vivo and degradation by extracts of the hypothalamus, anterior pituitary gland, lung, kidney, liver and plasma in vitro. In all cases, comparisons were made with synthetic LH-RH. When injected i.v. into mature ewes as a single dose, the potencies of the analogues were graded and Des Gly-NH210 LH-RH ethylamide was found to be the least potent. It was not possible to demonstrate any significant increase in the potency of this analogue over LH-RH, although a trend was apparent with each parameter examined. [d-Ser(But)6] Des Gly-NH210 LH-RH ethylamide had the greatest potency. There were no differences between the responses of anoestrous ewes and those of ewes treated on day 10 of the oestrous cycle. None of the analogues had a rate of elimination from the plasma different from that of LH-RH during either the first or the second components of the biphasic disappearance curve. The incubation of LH-RH with tissue extracts showed that extracts of the hypothalamus and anterior pituitary gland degraded LH-RH to a similar extent. Both the hypothalamic and anterior pituitary gland extracts degraded more LH-RH than did lung extract, which in turn destroyed more LH-RH than did extracts of kidney or liver tissue. The degradative abilities of kidney and liver extracts did not differ from each other. Plasma failed to degrade LH-RH or the analogues. Although LH-RH was rapidly destroyed by hypothalamic extract in vitro, of the analogues, only Des Gly-NH210 LH-RH ethylamide was degraded. The anterior pituitary gland and kidney extracts failed to degrade [d-Ser6] Des Gly-NH210 LH-RH ethylamide and [d-Ser(But)6] Des Gly-NH210 LH-RH ethylamide as rapidly as LH-RH. Extracts of liver and lung were incapable of catabolizing any of the analogues. There was an inverse correlation between the LH- and FSH-releasing potency of an analogue and its rate of degradation by anterior pituitary gland extract. The slower rates of catabolism of certain analogues of LH-RH by the anterior pituitary gland may explain their increased LH- and FSH-releasing potency.

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.

EFFECTS OF OESTRADIOL, HYPOTHALAMIC EXTRACTS AND LUTEINIZING HORMONE RELEASING HORMONE ON RAT ANTERIOR PITUITARY GLAND GONADOTROPHIN RELEASE IN VITRO BEFORE AND AFTER THE PREOVULATORY LUTEINIZING HORMONE SURGE AT PRO-OESTRUS

1981 ◽  
Vol 90 (3) ◽  
pp. 345-354 ◽  
Author(s):  
KATHLEEN A. ELIAS ◽  
C. A. BLAKE
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Anterior Pituitary Gland ◽  
Lh Surge ◽  
Releasing Hormone ◽  
Lh Rh ◽  
Lh Releasing Hormone

Changes at the anterior pituitary and/or hypothalamic levels which result in selective FSH release during late pro-oestrus in the cyclic rat were investigated. The possible involvement of decreasing serum concentrations of oestrogen during pro-oestrus in such changes was studied. Rats were decapitated at 12.00 h on pro-oestrus, before the onset of the LH surge and first phase of FSH release, or at 24.00 h on pro-oestrus, shortly after the onset of the second or selective phase of FSH release. Other rats were given oestrogen (OE2) at 14.00 h and killed at 24.00 h pro-oestrus. Paired hemi-anterior pituitary glands were incubated with vehicle or OE2 with or without synthetic LH-releasing hormone (LH-RH) or hypothalamic acid extracts prepared from rats killed at 12.00 or 24.00 h on pro-oestrus. At 24.00 h pro-oestrus, serum FSH concentration was high while serum LH concentration was low regardless of whether rats were given OE2. Glands collected and incubated at 24.00 h released more FSH and less LH than did glands collected and incubated at 12.00 h pro-oestrus. Administration of OE2 in vivo and/or in vitro did not affect these responses. The increments in LH and FSH release attributed to LH-RH or hypothalamic extracts in the glands incubated at 24.00 h were not different from those of the glands incubated at 12.00 h. Also, the hypothalamic extracts prepared from rats killed at 24.00 h were no more effective than the extracts prepared from rats killed at 12.00 h in releasing LH or FSH from glands incubated at 12.00 or 24.00 h pro-oestrus. Administration of OE2 in vivo caused a small suppression of LH-RH-induced FSH release. We suggest that a change occurs at the level of the anterior pituitary gland during the period of the LH surge and first phase of FSH release to increase basal FSH secretion selectively and cause, at least in part, the second phase of increased serum FSH. This change is not mediated by a decrease in serum oestrogen concentration. We failed to observe any evidence that LH-RH causes preferential FSH release during late pro-oestrus or that a hypothalamic peptide with a preferential FSH releasing ability is involved in FSH release at this time.

Role of serotonin in the control of secretion of corticotrophin releasing factor

1982 ◽  
Vol 93 (2) ◽  
pp. 151-160 ◽  
Author(s):  
M. C. Holmes ◽  
G. Di Renzo ◽  
U. Beckford ◽  
B. Gillham ◽  
M. T. Jones
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Synaptic Cleft ◽  
Anterior Pituitary Gland ◽  
Intraventricular Administration ◽  
Rat Hypothalamus ◽  
Corticotrophin Releasing Factor ◽  
The Status

The status of serotonin as a putative neurotransmitter involved in the control of the secretion of corticotrophin-releasing activity from the rat hypothalamus has been further investigated. The experimental model used for the investigation was the rat hypothalamus incubated in vitro. It was confirmed that serotonin causes a dose-related release of corticotrophin-releasing activity from the tissue and it was shown that this effect was mimicked by the addition to the tissue of chlorimipramine or d-fenfluramine, two drugs expected to cause an increase in the concentration of serotonin in the synaptic cleft. The effect of the latter drug was greatly reduced by the simultaneous addition of either methysergide or metergoline. Destruction of serotonin-containing nerve terminals in the hypothalamus was caused by the intraventricular administration of the neurotoxic drug 5,7-dihydroxytryptamine. This treatment resulted in an 84% reduction of the serotonin concentration in the hypothalamus 12 days later. Hypothalami taken from animals 12 days after treatment with the drug secreted corticotrophin-releasing activity in basal amounts equal to those found in tissues taken from control rats, but showed supersensitivity in response to added serotonin. No such supersensitivity was seen in response to d-fenfluramine and a diminished response to chlorimipramine was noted. Despite its intraventricular route of administration, 5,7dihydroxytryptamine was found to increase the sensitivity of segments of anterior pituitary gland in vitro to low doses of preparations containing corticotrophin releasing factor. These results are consistent with the view that endogenous serotonin can act as a stimulator of the secretion of corticotrophin-releasing activity from the rat hypothalamus. They also suggest that conclusions about the control of the release of this trophic material inferred from measurements of corticotrophin or corticosterone in the circulation must be viewed with caution when the drug 5,7-dihydroxytryptamine has been used, because of the development of supersensitivity both in the hypothalamus and in the anterior pituitary gland.

Further studies on the regulation, localization and function of the TRH-like peptide pyroglutamyl-glutamyl-prolineamide in the rat anterior pituitary gland

1995 ◽  
Vol 146 (2) ◽  
pp. 293-300 ◽  
Author(s):  
J M M Rondeel ◽  
W Klootwijk ◽  
E Linkels ◽  
P H M Jeucken, W ◽  
L J Hofland ◽  
...  
Keyword(s):  
Body Weight ◽  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Anterior Pituitary Gland ◽  
Female Rats ◽  
Pituitary Cells ◽  
Anterior Pituitary Cells ◽  
Lhrh Antagonist

Abstract Recent evidence shows that thyrotrophin-releasing hormone (TRH) immunoreactivity in the rat anterior pituitary gland is accounted for by the TRH-like tripeptide prolineamide-glutamyl-prolineamide (pGlu-Glu-ProNH2, <EEP-NH2). The present study was undertaken to investigate further the regulation, localization and possible intrapituitary function of <EEP-NH2. Anterior pituitary levels of <EEP-NH2 were determined between days 5 and 35 of life, during the oestrous cycle and after treatment with the luteinizing hormone-releasing hormone (LHRH) antagonist Org 30276. Treatment of adult males with the LHRH antagonist either for 1 day (500 μg/100 g body weight) or for 5 days (50 μg/100 g body weight) reduced anterior pituitary <EEP-NH2 levels by 25–30% (P<0·05 versus saline-treated controls). Anterior pituitary <EEP-NH2 increased between days 5 and 35 of life. In females, these levels were 2- to 3-fold higher (P<0·05) than in males between days 15 and 25 after birth; these changes corresponded with the higher plasma follicle-stimulating hormone (FSH) levels in the female rats. After day 25, <EEP-NH2 levels in female rats decreased in parallel with a decrease in plasma FSH. Injections with the LHRH antagonist (500 μg/100 g body weight), starting on day 22 of life, led to reduced contents of <EEP-NH2 in the anterior pituitary gland of female rats on days 26 and 30 (55 and 35% decrease respectively). Levels of <EEP-NH2 in the anterior pituitary gland did not change significantly during the oestrous cycle. Fractionation of anterior pituitary cells by unit gravity sedimentation was found to be compatible with the localization of <EEP-NH2 in gonadotrophs. In vitro, <EEP-NH2 dose-dependently inhibited TRH-stimulated growth hormone (GH) release from anterior pituitary cells obtained from neonatal rats, but no consistent effects were seen on the in vitro release of luteinizing hormone (LH), FSH, prolactin (PRL) or thyroid-stimulating hormone (TSH) under basal or TRH/LHRH-stimulated conditions. Furthermore, <EEP-NH2 did not affect the in vitro hormone release by anterior pituitary cells obtained from adult rats. In vivo, <EEP-NH2 (0·3–1·0 μg intravenously) did not affect plasma PRL, TSH, LH, FSH and GH in adult male rats. We conclude that <EEP-NH2 in the anterior pituitary gland is regulated by LHRH, is probably localized in gonadotrophs and may play a (paracrine) role in neonatal GH release. Journal of Endocrinology (1995) 146, 293–300

Effect of hypothalamic neuropeptides on corticotrophin release from quarters of rat anterior pituitary gland in vitro

1984 ◽  
Vol 100 (2) ◽  
pp. 219-226 ◽  
Author(s):  
S. A. Nicholson ◽  
T. E. Adrian ◽  
B. Gillham ◽  
M. T. Jones ◽  
S. R. Bloom
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Low Dose ◽  
Physiological Role ◽  
Anterior Pituitary Gland ◽  
High Concentration ◽  
Response Curves ◽  
Corticotrophin Releasing Factor ◽  
Basal Release

ABSTRACT The effect of six hypothalamic peptides on the basal release of ACTH and that induced by arginine vasopressin (AVP) or by ovine corticotrophin releasing factor (oCRF) from fragments of the rat anterior pituitary gland incubated in vitro was investigated. Dose–response curves to AVP and to oCRF were obtained, and the response to a low dose of oCRF was potentiated by a low dose of AVP. Basal release of ACTH was not affected by any of the peptides in concentrations in the range 10−12 to 10−6 mol/l, and only substance P (SP) and somatostatin (SRIF) inhibited significantly the response to oCRF in a dose-related manner. The responses to a range of doses of oCRF or AVP were reduced by 10−8 and 10 − 6 mol SP or SRIF/1, and to a greater extent by the higher dose. Except in the case of 10−6 mol SRIF/1 on the response to AVP, the response was not further diminished by preincubation of the tissue with the peptide before the stimulating agent was added. The inhibition of the responses to AVP or oCRF by 10−9 mol SP/1 was not potentiated by its combination with either 5 × 10−10 or 10−8 mol SRIF/1; the inhibitory effects were merely additive. The results suggest that although SRIF and SP are able to modulate the release of ACTH from the anterior pituitary gland, they do so only at a high concentration. In the case of SRIF these concentrations are several orders of magnitude higher than those reported to be present in the hypophysial portal blood and therefore a physiological role for this peptide in the control of ACTH secretion is unlikely. J. Endocr. (1984) 100, 219–226

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