Effects of the opioid antagonist naloxone on release of luteinizing hormone in mares during the anovulatory season

1994 ◽  
Vol 142 (1) ◽  
pp. 139-144 ◽  
Author(s):  
C Aurich ◽  
S Schlote ◽  
H-O Hoppen ◽  
E Klug ◽  
H Hoppe ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Anterior Pituitary ◽  
Reproductive Activity ◽  
Endogenous Opioids ◽  
Opioid Antagonist ◽  
Lh Release ◽  
Lh Secretion ◽  
Opioid Systems ◽  
Follicular Activity

Abstract To investigate an involvement of endogenous opioids in the regulation of circannual changes in reproductive activity, effects of the opioid antagonist naloxone on the concentration of immunoreactive and bioactive luteinizing hormone (LH) in plasma were measured in mares during the anovulatory season. Naloxone (0·5 mg/kg i.v.) caused a significant increase (P<0·05) in immunoreactive as well as bioactive LH concentration in plasma. The amplitude of the increase in LH concentrations measured with an in vitro bioassay was more pronounced than the amplitude of the increase in LH secretion determined by radioimmunoassay. This indicates that although in seasonal anovulatory mares the bioactivity of LH in plasma is low, highly bioactive LH is present in the anterior pituitary and can be released by naloxone. The LH response to naloxone did not depend on the degree of ovarian follicular activity. It can be concluded that a tonic opioid inhibition of LH release is present in mares during at least part of the anovulatory season and that endogenous opioids seem to be involved in the regulation of seasonal reproductive activity in the horse. In contrast to the situation during the breeding season, the opioid systems regulating LH release are activated independently of luteal progesterone. Journal of Endocrinology (1994) 142, 139–144

Oxytocin modulates the luteinizing hormone response of the rat anterior pituitary to gonadotrophin-releasing hormone in vitro

1995 ◽  
Vol 145 (1) ◽  
pp. 113-119 ◽  
Author(s):  
J J Evans ◽  
S J Hurd ◽  
D R Mason
Keyword(s):  
Luteinizing Hormone ◽  
Anterior Pituitary ◽  
The Self ◽  
Female Rats ◽  
Hormone Response ◽  
Priming Process ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone ◽  
Lh Secretion

Abstract Although GnRH is believed to be the primary secretagogue for LH, oxytocin has also been shown to stimulate LH release from the anterior pituitary. We investigated the possibility that the two secretagogues interact in the modulation of LH release. Anterior pituitaries were removed from adult female rats at pro-oestrus, and tissue pieces were pre-incubated in oxytocin for 3 h prior to being stimulated with 15 min pulses of GnRH. LH output over the 1 h period from the beginning of the GnRH pulse was determined. Control incubations were carried out in the absence of oxytocin, and background secretory activities without GnRH stimulation were also determined. Tissue which was pre-exposed to oxytocin (0·012–1·25 μm) had an increased LH response to GnRH (1·25 nm). The increase was larger than the sum of the LH outputs obtained with oxytocin and GnRH separately, revealing that oxytocin synergistically enhanced LH secretion elicited by GnRH (P<0·05; ANOVA). If stimulation by GnRH was delayed for 2 h after incubation with oxytocin, an increase in LH secretion was still observed, indicating that oxytocin-induced modulation did not rapidly disappear. Oxytocin pre-incubation was observed to result in an increase of maximal GnRH-induced LH output (P<0·001; t-test), as well as an increase of intermediate responses. The LH response of the anterior pituitary to subsequent pulses of GnRH was modified by the self-priming process. The effect of oxytocin pretreatment on the response of primed tissue to GnRH was also investigated. It was found that pre-incubation in oxytocin also enhanced the LH response of primed tissue to GnRH. The study has revealed that oxytocin increases the LH output of anterior pituitary tissue in response to GnRH. The effect occurs on both GnRH-primed and unprimed tissues. The results suggest that oxytocin has the potential to regulate the dynamics of the pro-oestrous LH surge. Journal of Endocrinology (1995) 145, 113–119

Stimulatory effect of thyrotrophin-releasing hormone (TRH) on the release of luteinizing hormone (LH) from rat anterior pituitary cells in vitro

1983 ◽  
Vol 61 (2) ◽  
pp. 186-189 ◽  
Author(s):  
Noboru Fujihara ◽  
Masataka Shiino
Keyword(s):  
Luteinizing Hormone ◽  
Anterior Pituitary ◽  
Pituitary Cells ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Anterior Pituitary Cells ◽  
Lh Release ◽  
Lh Rh

The effect of thyrotrophin-releasing hormone (TRH, 10−7 M) on luteinizing hormone (LH) release from rat anterior pituitary cells was examined using organ and primary cell culture. The addition of TRH to the culture medium resulted in a slightly enhanced release of LH from the cultured pituitary tissues. However, the amount of LH release stimulated by TRH was not greater than that produced by luteinizing hormone – releasing hormone (LH–RH, 10−7 M). Actinomycin D (2 × 10−5 M) and cycloheximide (10−4 M) had an inhibitory effect on the action of TRH on LH release. The inability of TRH to elicit gonadotrophin release from the anterior pituitary glands in vivo may partly be due to physiological inhibition of its action by other hypothalamic factor(s).

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.

scholarly journals Effects of Central Injection of Anti-LPS Antibody and Blockade of TLR4 on GnRH/LH Secretion during Immunological Stress in Anestrous Ewes

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Karolina Haziak ◽  
Andrzej Przemysław Herman ◽  
Dorota Tomaszewska-Zaremba
Keyword(s):  
Luteinizing Hormone ◽  
Anterior Pituitary ◽  
Gonadotropin Releasing Hormone ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Immune Stress ◽  
Immunological Stress ◽  
Lh Release ◽  
Lh Secretion ◽  
Tlr4 Receptor

The present study was designed to examine the effect of intracerebroventricular (icv) administration of antilipopolysaccharide (LPS) antibody and blockade of Toll-like receptor 4 (TLR4) during immune stress induced by intravenous (iv) LPS injection on the gonadotropin-releasing hormone/luteinizing hormone (GnRH/LH) secretion in anestrous ewes. Injection of anti-LPS antibody and TLR4 blockade significantly (P < 0.01) reduced the LPS dependent lowering amount ofGnRHmRNA in the median eminence (ME). Moreover, blockade of TLR4 caused restoration ofLH-βtranscription in the anterior pituitary decreased by the immune stress. However, there was no effect of this treatment on reduced LH release. The results of our study showed that the blockade of TLR4 receptor in the hypothalamus is not sufficient to unblock the release of LH suppressed by the immune/inflammatory challenges. This suggests that during inflammation the LH secretion could be inhibited directly at the pituitary level by peripheral factors such as proinflammatory cytokines and circulating endotoxin as well.

Effect of calcium and potassium on basal and gonadotrophin-releasing hormone (GnRH) stimulated release of luteinizing hormone (LH)

1981 ◽  
Vol 97 (1) ◽  
pp. 26-32 ◽  
Author(s):  
Joseph C. Zolman ◽  
Lubomir J. Valenta
Keyword(s):  
Luteinizing Hormone ◽  
Anterior Pituitary ◽  
Potassium Concentration ◽  
Extracellular Calcium ◽  
Tissue Slices ◽  
In Vitro Superfusion ◽  
Potassium Effect ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone

Abstract. LH release from the anterior pituitary was studied by the method of an in vitro superfusion of bovine anterior pituitary tissue slices. LH release was stimulated by increased potassium concentration (23 and 59 mm) and by synthetic GnRH (1 and 4 ng/ml). While the potassium effect was completely dependent on extracellular calcium, that of GnRH was only partially dependent. Additive effect was observed when GnRH followed enhanced potassium infusion but not vice versa. This suggested that the mechanism responding to potassium may be contained within the stimulatory pathway of GnRH. There was a difference in the dynamics of the LH response: maximum response was attained in about 10 min of potassium infusion while infusion of GnRH resulted mostly in multiphasic stepwise release of LH reaching a plateau in 60 to 90 min only. It is speculated that the potassium effect involves the K+, Na+ dependent ATPase.

cAMP augmentation of secretagogue-induced luteinizing hormone secretion

1986 ◽  
Vol 250 (1) ◽  
pp. E62-E68 ◽  
Author(s):  
J. L. Turgeon ◽  
D. W. Waring
Keyword(s):  
Luteinizing Hormone ◽  
Hormone Secretion ◽  
Base Line ◽  
Luteinizing Hormone Secretion ◽  
Secretory Rate ◽  
Camp Analogue ◽  
Lh Release ◽  
Lh Secretion ◽  
Camp Elevation

Whether adenosine 3',5'-cyclic monophosphate (cAMP) acts as a mediator for luteinizing hormone-releasing hormone (LHRH) in either its immediate LH release action or in its self-priming action was investigated. Pituitary pieces from either proestrous or estrous rats were superfused in vitro in the presence of dibutyryl cAMP [(Bu)2cAMP], 8-bromo-cAMP (8BrcAMP), forskolin, or control for 2-3 h. For proestrous but not estrous pituitary pieces, a slight increase in base-line LH secretion rate occurred at approximately 70 min of exposure to elevated cAMP; in the same system LHRH caused an increase in LH secretory rate within 2 min in either proestrous or estrous tissue. In contrast to its ineffectiveness as a secretagogue, cAMP elevation resulted in a severalfold augmentation of both LHRH- and elevated K+-induced LH secretion from proestrous but not estrous pituitary pieces; for these experiments, superfusion with a cAMP analogue or forskolin for varying times preceded a 10-min pulse of either 8 nM LHRH or 47 mM K+. Augmentation was evident after 30 min of cAMP elevation; longer exposures were coincident with greater potentiation. Cycloheximide prevented (Bu)2cAMP augmentation of LHRH-induced secretion. These data show that cAMP does not mediate the immediate LH release action of LHRH, but cAMP does augment LHRH- or K+-induced LH secretion with characteristics in common with the self-priming action of LHRH.

Effect of GnRH and its antagonist (Antarelix) on LH release from cultured bovine anterior pituitary cells

2002 ◽  
Vol 50 (1) ◽  
pp. 79-92 ◽  
Author(s):  
Annett Bellmann ◽  
F. Schneider ◽  
W. Kanitz ◽  
Keyword(s):  
Anterior Pituitary ◽  
Culture System ◽  
Gnrh Antagonist ◽  
Pituitary Cells ◽  
Maximal Effect ◽  
Static Culture ◽  
Lh Release ◽  
Lh Secretion

In the following investigations, the LH secretion of cells from pituitaries in heifers on days 16-18 of their oestrous cycle (n = 14) was analysed. Cells were dissociated with trypsin and collagenase and maintained in a static culture system. For the estimation of LH release, the cells were incubated with various concentrations of mammalian GnRH (Lutrelef) for 6h. To determine the action of Antarelix (GnRH antagonist), the cells were preincubated for 1 h with concentrations of 10-5 or 10-4 M Antarelix followed by 10-6 M GnRH coincubation for a further 6h. At the end of each incubation, the medium was collected for LH analysis. Parallel, intracellular LH was qualitatively detected by immunocytochemistry. Changes in the intensity of LH staining within the cells in dependence of different GnRH concentrations were not observed, but a significant increase LH secretion in pituitary cells was measured at 10-6 M GnRH. Antarelix had no effect on basal LH secretion at concentrations of 10-4 and 10-5 M. After coincubation of pituitary cells with Antarelix and GnRH, Antarelix blocked the GnRH-stimulated LH secretion with a maximal effect of 10-4 M, but the staining of immunoreactive intracellular LH was detected at approximately the same level compared to the pituitary cells treated with exogenous GnRH alone. These data demonstrate that Antarelix is effective in influencing the GnRH-stimulated LH secretion of pituitary cells in vitro. After administration of Antarelix in vivo, the GnRH-stimulated LH secretion of cultured pituitary cells was not inhibited.

Synthesis and release of luteinizing hormone in vitro: manipulations of Ca2+ environment

1985 ◽  
Vol 249 (2) ◽  
pp. E165-E174
Author(s):  
T. C. Liu ◽  
G. L. Jackson
Keyword(s):  
Luteinizing Hormone ◽  
Total Protein ◽  
Anterior Pituitary ◽  
Gonadotropin Releasing Hormone ◽  
Total Cell ◽  
Ionophore A23187 ◽  
Pituitary Cells ◽  
Free Medium ◽  
Lh Release

We determined if luteinizing hormone (LH) synthesis is Ca2+ dependent and coupled to LH release. We monitored LH synthesis when LH release was stimulated either by specific [gonadotropin-releasing hormone (GnRH)] or nonspecific stimuli (50 mM K+ and 2 or 20 microM Ca2+ ionophore A23187) and inhibited by Ca2+-reduced medium. LH synthesis was estimated by measuring incorporation of [3H]glucosamine (glycosylation) and [14C]alanine (translation) into total (cell and medium) immunoprecipitable LH by cultured rat anterior pituitary cells. Both GnRH (1 nM) and 50 mM K+ significantly stimulated LH release and glycosylation, but had no effect on LH translation. A23187 also stimulated LH release, but significantly depressed glycosylation of LH and total protein and [14C]alanine uptake. Deletion of Ca2+ from the medium depressed both GnRH-induced LH release and glycosylation. Addition of 0.1 mM EGTA to Ca2+-free medium not only inhibited GnRH-induced release and glycosylation of LH but also uptake of precursors and glycosylation and translation of total protein. Thus glycosylation and release of LH are Ca2+ dependent. Whether parallel changes in LH release and glycosylation reflect a cause and effect relationship remains to be determined.

Suppression by LRH of the stimulatory effect of oestradiol on the secretion of LH by the rat pituitary gland

1987 ◽  
Vol 114 (4) ◽  
pp. 488-496
Author(s):  
G. A. Schuiling ◽  
H. Moes ◽  
J. de Koning ◽  
T. R. Koiter
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Secretion Rate ◽  
Ovariectomized Rats ◽  
Release Mechanisms ◽  
Lh Release ◽  
Lh Secretion ◽  
Positive Effect

Abstract. Ovariectomized rats were infused with varying doses of luteinizing hormone-releasing-hormone (LRH). Some of the rats were also treated with oestradiol benzoate (EB). The effects of these pre-treatments on the in vitro release of luteinizing hormone (LH) were studied. The following parameters of in vitro LH release were measured: a) the autonomous secretion rate; b) the secretion rate following maximum stimulation with LRH, and c) the total quantity of LH released during the 6-hour experiment. The in vivo pre-treatments with LRH and EB dose-dependently decreased the pituitary LH content as well as all three of the above parameters of in vitro LH secretion. There was a linear relationship between the pituitary LH content and the three parameters of in vitro LH release. These parameters were therefore expressed as percentage of the pituitary LH content to give the relative LH secretion rates. The three parameters were thereby corrected for LRH/EB-induced changes in the pituitary LH content. In this way we obtained information on the effects of LRH and EB on the state of the LH release mechanisms of the gonadotropes. EB potentiated the LRH-induced depletion of the pituitary LH stores at all in vivo LRH infusion rates. The effect of EB on the quantity of LH released during perifusion in vitro, however, varied with the previous LRH infusion rates. After LRH infusion rates lower than about 120 ng/h (which establishes plasma concentrations of about 70 ng/l) EB enhanced the stimulated quantity of LH released. After higher rates of LRH infusion, EB lowered the amount of LH released. The effect of EB on the relative secretion of LH in vitro, i.e. on the LH release mechanisms, however, was positive irrespective of the prior in vivo LRH infusion rates, although the effect of EB was greater at the lower rates of LRH infusion. The effect of EB on the autonomous, in vitro, LH secretion rate was positive irrespective of the prior in vivo LRH infusion rates. The positive effect of EB on the mechanism underlying this component of LH secretion was LRH-independent. The effect of EB on the mechanism underlying the LRH-stimulated component of LH release appeared to be strongly LRH-dependent. The effect of EB was maximal if the LRH infusion rate had been lower than about 50 ng/h. With higher infusion rates it became increasingly smaller and was zero at the rate of about 180 ng/h or more. The LRH infusion rates of 50 and 180 ng/h establish plasma LRH concentrations of about 30 and 90 ng/l. Thus, the positive effect of EB on the LRH-stimulated component of LH secretion can be regulated by LRH at the plasma concentration interval of 30–90 ng/l. This study demonstrates that the 'overall' effect of EB on the LH secretion rate is determined by the 'balance' between the effect of EB on the pituitary LH content (the potentiation of the LRH-induced depletion of the LH stores) and the effect of EB on the LH release mechanisms (which effect, in the case of the LRH-stimulated component of LH secretion, can be suppressed by LRH). If the former effect dominates, the effect of EB on the secretion of LH is negative, if the latter dominates, the effect of EB is positive. The LRH concentration at which the positive effect turns into the negative effect is about 70 ng/l. We suggest that the ability of LRH and EB to influence each others' effect on the pituitary gland at physiological concentrations of the two hormones, plays a role in the regulation of the secretion of LH.

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