Dynamic changes in pituitary responses to luteinizing hormone releasing hormone after ovariectomy in the rat

1982 ◽  
Vol 93 (1) ◽  
pp. 75-81 ◽  
Author(s):  
S. A. Whitehead ◽  
J. M. Pennington ◽  
D. A. Carter
Keyword(s):  
Luteinizing Hormone ◽  
Significant Rise ◽  
Dynamic Changes ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
The Third ◽  
Lh Rh ◽  
Lh Releasing Hormone ◽  
Perifusion System

Changes in pituitary responses to pulses of LH releasing hormone (LH-RH) after ovariectomy in the rat have been investigated with an in-vitro perifusion system. On the third day after ovariectomy there was a large increase in the responsiveness of the pituitary gland to LH-RH compared with days 1 and 2 and this preceded the first significant rise in circulating concentrations of LH. Exaggerated responses were observed on all subsequent days tested (days 4, 6, 10, 18 and 28) although the size of the response on day 10 was significantly lower compared with days 6, 18 or 28. It is suggested that the early phase of increased pituitary responsiveness to LH-RH results from a rise in pituitary LH-RH receptors, which increases both the synthesis of LH and the response to exogenous LH-RH. The reduced LH response, measured on day 10, may correlate with an increase in the endogenous secretion of LH-RH and an imbalance between LH synthesis and secretion at this time.

Effects of chronic treatment with oestrogen, an oestrogen antagonist and a potent luteinizing hormone releasing hormone agonist analogue on pituitary responsiveness to luteinizing hormone releasing hormone in the rat

1983 ◽  
Vol 98 (3) ◽  
pp. 313-321 ◽  
Author(s):  
J. M. Hall ◽  
S. A. Whitehead
Keyword(s):  
Luteinizing Hormone ◽  
Chronic Treatment ◽  
Ex Vivo ◽  
Significant Rise ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Serum Lh ◽  
Lh Release ◽  
Lh Releasing Hormone

The rise in gonadotrophin release which occurs after ovariectomy is caused by steroid withdrawal resulting in an enhanced pituitary responsiveness to LH releasing hormone (LHRH) associated with increased LHRH release and pituitary LHRH binding. The effects of oestrogen replacement after ovariectomy and chronic treatment of intact rats with an oestrogen antagonist, tamoxifen, on LH release and in-vitro pituitary responses to LHRH have been investigated. Capsules containing crystalline oestradiol, implanted at the time of ovariectomy, completely inhibited the rise in LH release although pituitary responsiveness was greater after 10 days in the oestrogen-treated rats than in untreated ovariectomized controls. On day 4 after ovariectomy pituitary responses to LHRH were comparable in both treated and untreated groups although in both groups the responses were greater than those measured in intact dioestrous rats. Treatment with tamoxifen over a 4-day period also augmented pituitary responsiveness but only at the lowest dose (0·5 mg/kg); no effect on serum LH concentrations was observed. Higher doses of the antagonist (1 and 2 mg/kg) did not affect pituitary responses, although the highest dose did cause a significant rise in serum LH. Treatment with a daily dose of 50 ng [d-Ser(But)6]LHRH(1–9)nonapeptide-ethylamide, starting on the day of ovariectomy, markedly attenuated the LH responses to LHRH ex vivo at days 2, 4 and 10 after ovariectomy. In contrast, the analogue treatment did not abolish the rise in LH release but this was proportionately less than in controls.

EFFECT OF CORTISOL OR ADRENOCORTICOTROPHIN ON RELEASE OF LUTEINIZING HORMONE INDUCED BY LUTEINIZING HORMONE RELEASING HORMONE IN THE DAIRY HEIFER

1982 ◽  
Vol 92 (1) ◽  
pp. 141-146 ◽  
Author(s):  
R. L. MATTERI ◽  
G. P. MOBERG
Keyword(s):  
Luteinizing Hormone ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Dairy Heifers ◽  
Significant Difference ◽  
Significant Depression ◽  
Lh Rh ◽  
Lh Releasing Hormone ◽  
And Control ◽  
Slight Depression

During treatment with cortisol or ACTH, dairy heifers were given two doses of LH releasing hormone (LH-RH) spaced 1·5 h apart. Serum concentrations of cortisol and LH were monitored during each treatment. Treatment with both ACTH and cortisol raised plasma cortisol levels above the respective saline controls (P<0·001). Neither treatment affected basal LH concentrations. A slight depression in LH response was seen in the cortisol-treated animals after the first LH-RH injection, as shown by a statistically significant depression at three of the sample times. There was no significant difference between treated and control LH values after the second LH-RH administration. Treatment with ACTH resulted in significantly reduced LH values at all sample times after both injections of LH-RH.

Antagonistic activity of analogs of luteinizing hormone-releasing hormone (LH-RH) in vitro

1976 ◽  
Vol 5 (3-4) ◽  
pp. 201-208 ◽  
Author(s):  
D.H. Coy ◽  
F. Labrie ◽  
M. Savary ◽  
E.J. Coy ◽  
A.V. Schally
Keyword(s):  
Luteinizing Hormone ◽  
Antagonistic Activity ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Lh Rh

STIMULATION OF PROSTAGLANDIN ACCUMULATION IN THE RAT ANTERIOR PITUITARY GLAND BY LUTEINIZING HORMONE RELEASING HORMONE IN VITRO

1977 ◽  
Vol 75 (2) ◽  
pp. 277-283 ◽  
Author(s):  
N. BARDEN ◽  
A. BETTERIDGE
Keyword(s):  
Luteinizing Hormone ◽  
Cyclic Amp ◽  
Anterior Pituitary ◽  
Pituitary Cells ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Lh Release ◽  
Lh Rh ◽  
Stimulation Of

The addition of luteinizing hormone releasing hormone (LH-RH) to cultures of monolayers of rat anterior pituitary cells was shown to increase both the concentrations of prostaglandins E1 and E2 (PGE) in the cells and the release of LH over similar ranges of concentrations of LH-RH (10−6 to 10−10 mol/l). The peak concentration of PGE was observed after 2·5 h. The stimulation of the level of PGE in the cells by LH-RH was completely inhibited by two inhibitors of prostaglandin synthetase, which only partially inhibited the stimulation of LH release. Therefore the increased concentration of PGE was not obligatory for the effect of LH-RH on LH release. It was also shown that monobutyryl cyclic AMP stimulated the intracellular concentration of PGE and it is suggested that the stimulation of PGE levels may be mediated by increased levels of cyclic AMP in the cells after the addition of LH-RH.

Serotonin induces gonadotrophin release through stimulation of LH-releasing hormone release from the median eminence

1986 ◽  
Vol 111 (2) ◽  
pp. 309-315 ◽  
Author(s):  
M. L. Vitale ◽  
M. N. Parisi ◽  
S. R. Chiocchio ◽  
J. H. Tramezzani
Keyword(s):  
Median Eminence ◽  
Anterior Pituitary ◽  
Female Rats ◽  
Male Rats ◽  
Tissue Samples ◽  
Releasing Hormone ◽  
The Third ◽  
Lh Releasing Hormone ◽  
Perifusion System

ABSTRACT The effects of serotonin (5-HT) on the release of gonadotrophins and LH-releasing hormone (LHRH) were examined in an in-vitro perifusion system using median eminences and/or anterior pituitaries obtained from male or pro-oestrous female rats. Animals were killed by decapitation between 12.00 and 13.00 h. A serial double-chamber perifusion system was employed. Three types of experiments were performed. In the first, median eminences were placed in the first chamber and one anterior pituitary in the second chamber. In the second group, only the anterior pituitary was perifused. In the third group, only five median eminences were perifused. In the first and second experiments, LH, FSH and prolactin were determined in the perifusion efflux by radioimmunoassay (RIA). In the third experiment, LHRH was determined by RIA. Addition of 5-HT (final concentrations 0·06, 0·6 and 6·0μmol/l) into the first chamber containing the median eminences stimulated the release of LH and FSH from the pituitary, but did not affect the levels of prolactin in the effluent in the same experiment (prooestrous rats). The stimulatory effect of 5-HT was blocked by the addition of cyproheptadine (1 μmol/l) in the perifusion fluid. The introduction of 5-HT (0·6 μmol/l) into the tube connecting the first and second chambers did not modify the release of LH, nor did 5-HT added to the pituitaries perifused alone. Injection of 5-HT into the first chamber (median eminences), containing tissue samples from male rats, stimulated LH release, but to a significantly (P< 0·001) lower degree than that found when samples from pro-oestrous females were used (P< 0·0001). When median eminences from pro-oestrous rats were perifused alone, injection of 5-HT produced an immediate release of LHRH which peaked during the first 10 min of collection and lasted for 30 min; in these experiments, a clear relationship existed between dose of 5-HT and release of LHRH (P<0·02). The stimulatory effect of 5-HT was blocked by the addition of cyproheptadine (5 μmol/l) or methiothepin (5 μmol/l). These results demonstrate that 5-HT stimulates gonadotrophin release by acting directly on LHRH terminals in the median eminence from pro-oestrous rats. Furthermore, the effect of 5-HT on LHRH release was dose dependent and was nullified by 5-HT receptor blockers (cyproheptadine and methiothepin). J. Endocr. (1986) 111, 309–315

APPLICATION OF AN IN-VITRO PERIFUSION TECHNIQUE TO STUDIES OF LUTEINIZING HORMONE RELEASE BY RAT ANTERIOR HEMI-PITUITARIES: SELF-POTENTIATION BY LUTEINIZING HORMONE RELEASING HORMONE

1976 ◽  
Vol 68 (2) ◽  
pp. 197-207 ◽  
Author(s):  
J. A. EDWARDSON ◽  
D. GILBERT
Keyword(s):  
Luteinizing Hormone ◽  
Priming Effect ◽  
Hormone Release ◽  
Physiological Control ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Hypothalamic Extract ◽  
Lh Rh ◽  
Lh Secretion

SUMMARY A technique is described for the continuous perifusion of rat adenohypophyses. Exposure of the perifused glands to repeated equal 5 min stimuli with hypothalamic extract resulted in a series of equal peaks of corticotrophin secretion, the response was proportional to log dose over the range 0·25–2·0 rat hypothalamic equivalents/ml. Repeated equal stimuli with hypothalamic extract, or with luteinizing hormone releasing hormone (LH-RH) at concentrations of 2 or 10 ng/ml, resulted in a progressively increasing series of peaks of LH secretion, i.e. a self-potentiating or priming effect. The effect took between 30 min and 1 h to develop. A delayed increase in the responsiveness of the glands was also seen with continuous incubation of anterior pituitaries with LH-RH. The relevance of these observations to the physiological control of LH secretion is discussed.

Comparison of pharmacological effect of adiphenine and physiological stimulation by luteinizing hormone releasing hormone on luteinizing hormone release by rat anterior pituitaries in vitro

1979 ◽  
Vol 57 (12) ◽  
pp. 1388-1392 ◽  
Author(s):  
M. Fevre ◽  
D. Jordan ◽  
J. Tourniaire ◽  
R. Mornex
Keyword(s):  
Luteinizing Hormone ◽  
Dependent Manner ◽  
Similar Time ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Calcium Dependent ◽  
Lh Release ◽  
Time Courses ◽  
Lh Rh

The mechanism of action of adiphenine on in vitro rat anterior pituitary LH release was studied and compared with that of the physiological stimulator luteinizing hormone releasing hormone (LH-RH) on LH release. The comparative study showed that adiphenine and LH-RH were able to increase medium LH concentration in a dose-dependent manner and had similar time courses of action between 1 and 4 h incubation. However, there were several main differences between the effects of adiphenine and LH-RH. The adiphenine action was not calcium dependent, was inhibited in a high K+ medium concentration, and was substituted after energy depression. It is concluded that adiphenine probably acts near the ultimate steps of the LH release pathway and could be a useful pharmacological tool for studying the mechanism of LH release.

Priming effect of luteinizing hormone releasing hormone in the hypogonadal mouse

1982 ◽  
Vol 94 (2) ◽  
pp. 283-287 ◽  
Author(s):  
G. Fink ◽  
W. J. Sheward ◽  
H. M. Charlton
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Priming Effect ◽  
Plasma Concentrations ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Lh Rh ◽  
Lh Releasing Hormone

We have investigated the LH response to LH releasing hormone (LH-RH) in female hypogonadal (hpg) mice in which the hypothalamus contains no LH-RH and the pituitary gland contains significantly less LH than in normal mice. Both the releasing action and the priming effect of LH-RH were not significantly different in hpg compared with normal mice. Raised plasma concentrations of oestradiol-17β reduced pituitary responsiveness to LH-RH in normal but not in hpg mice. These results show that in the mouse neither longterm exposure to normal levels of LH-RH nor a normal pituitary content of LH are necessary for either the releasing or the priming action of LH-RH.

Plasma cortisol response to thyrotrophin releasing hormone and luteinizing hormone releasing hormone in healthy kennel dogs and in dogs with pituitary-dependent hyperadrenocorticism

1982 ◽  
Vol 93 (3) ◽  
pp. 365-369 ◽  
Author(s):  
R. Stolp ◽  
R. J. M. Croughs ◽  
J. C. Meijer ◽  
A. Rijnberk
Keyword(s):  
Plasma Concentration ◽  
Luteinizing Hormone ◽  
Intravenous Injection ◽  
Plasma Cortisol ◽  
Cortisol Response ◽  
Thyrotrophin Releasing Hormone ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Lh Rh ◽  
Lh Releasing Hormone

The change in the plasma concentration of cortisol after the administration of thyrotrophin releasing hormone (TRH) and LH releasing hormone (LH-RH) was studied in normal dogs and in dogs with pituitary-dependent hyperadrenocorticism (PDH). The normal dogs showed a small but significant increase in the plasma concentration of cortisol 15 min after intravenous injection of TRH and LH-RH. In ten of the dogs with PDH the response to TRH was not significantly different from that in the normal dogs, but in 13 the response was significantly greater. In 15 of the dogs with PDH the response to LH-RH administration was within or below the range of responses in the normal dogs and in only one dog was the response to LH-RH greater than that in the normal dogs. These findings are discussed in relation to the pathogenesis of PDH.

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