LUTEINIZING HORMONE RELEASING HORMONE-INDUCED RELEASE OF LUTEINIZING HORMONE FROM PITUITARY EXPLANTS OF COWS KILLED BEFORE OR AFTER OESTRADIOL TREATMENT

1981 ◽  
Vol 88 (1) ◽  
pp. 17-25 ◽  
Author(s):  
E. M. CONVEY ◽  
J. S. KESNER ◽  
V. PADMANABHAN ◽  
T. D. CARRUTHERS ◽  
T. W. BECK
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Lh Surge ◽  
Releasing Hormone ◽  
Oestradiol Treatment ◽  
Readily Releasable Pool ◽  
Serum Lh ◽  
Pituitary Glands ◽  
Lh Rh ◽  
Lh Releasing Hormone

In ovariectomized heifers, oestradiol decreases concentrations of LH in serum for approximately 12 h after which LH is released in a surge comparable in size and duration to the preovulatory surge. Using this model, we measured LH release induced by LH releasing hormone (LH-RH) from pituitary explants taken from ovariectomized heifers before or after an oestradiol-induced LH surge. These changes were related to changes in LH concentrations in serum and pituitary glands and hypothalamic LH-RH content. Twenty Holstein heifers were randomly assigned to one of four treatment groups to be killed 0, 6, 12, or 24 h after the injection of 500 μg oestradiol-17β. Jugular blood was collected at −2, −1 and 0 h then at intervals of 2 h until slaughter. Pituitary glands were collected and ≃2 mm3 explants were exposed to 4 ng LH-RH/ml medium for 30 min (superfusion) or 4 ng LH-RH/ml medium for 2 h in Erlenmeyer flasks. Levels of LH were measured in the medium. Hypothalami, collected at autopsy, were assayed for LH-RH content. To determine pituitary LH content, an additional 15 ovariectomized heifers were killed, five each at 0, 12 and 24 h after the injection of 500 μg oestradiol. In both groups of heifers, oestradiol reduced serum LH concentrations to ≃ 1 ng/ml, a level which persisted for 12 h, when LH was released in a surge. Pituitary sensitivity to LH-RH was increased at 6 and 12 h after the injection of oestradiol, but was markedly decreased at 24 h, i.e. after the LH surge. Despite this twofold increase in capacity of the pituitary gland to release LH in response to LH-RH, pituitary LH content did not change during 12 h after oestradiol treatment. However, LH content decreased after the LH surge and this decrease was associated with a decrease in pituitary responsiveness to LH-RH. Hypothalamic LH-RH content was not altered by these treatments. We have interpreted our results as evidence that oestradiol exerts a positive feedback effect on the pituitary gland of ovariectomized heifers such that pituitary sensitivity to LH-RH is increased twofold by the time the LH surge is initiated. In addition, oestradiol causes a transitory inhibition of LH-RH release as shown by the fact that serum LH concentrations remained low during the interval from injection of oestradiol until the beginning of the LH surge despite the fact that pituitary sensitivity to LH-RH is increased at this time. Depletion of a readily releasable pool of pituitary LH may be the mechanism by which the LH surge is terminated.

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.

STIMULATION OF RELEASE OF LUTEINIZING HORMONE FROM CULTURED PITUITARY CELLS BY 2- AND 4-HYDROXYLATED OESTROGENS

1981 ◽  
Vol 90 (3) ◽  
pp. 433-436 ◽  
Author(s):  
S. FRANKS ◽  
G. R. MERRIAM ◽  
CYNTHIA G. GOODYER ◽  
F. NAFTOLIN
Keyword(s):  
Luteinizing Hormone ◽  
Anterior Pituitary ◽  
Monolayer Culture ◽  
Pituitary Cells ◽  
Releasing Hormone ◽  
Oestradiol Treatment ◽  
Lh Rh ◽  
Lh Releasing Hormone ◽  
Stimulation Of

We have examined the effects of the catechol oestrogens 2-hydroxyoestradiol (2-OHE2), 4-hydroxyoestradiol (4-OHE2) and 2-hydroxyoestrone (2-OHE1) and their corresponding primary oestrogens on secretion of LH and FSH by enzymatically dispersed rat anterior pituitary cells in monolayer culture. Basal LH levels in the medium were significantly higher than in control wells when cells were exposed to 10−8m-oestradiol-17β for 40 h: oestrone and all three catechol oestrogens (in the same doses) also stimulated basal LH concentrations to levels quantitatively similar to those seen after oestradiol treatment. The same effects were observed when steroids were given at 10−9 mol/l. Oestradiol, 2-OHE2, and 4-OHE2 but not 2-OHE1 increased pituitary responsiveness to LH releasing hormone (LH-RH) (given in a range of doses from 10−11 to 10−6 mol/l). The responses of cells treated with 2-OHE2 and 4-OHE2 were similar, though less than the response seen after treatment with oestradiol. This contrasts with the very different oestrogenic effects of 2- and 4-OHE2 previously observed in vivo. Neither oestradiol nor the catechol oestrogens had any effect on basal or LH-RH-stimulated FSH release.

DEPENDENCE ON PROTEIN SYNTHESIS OF THE N6-MONOBUTYRYL CYCLIC AMP PLUS THEOPHYLLINE MEDIATED RELEASE OF LUTEINIZING HORMONE INDUCED BY LUTEINIZING HORMONE RELEASING HORMONE FROM RAT PITUITARY GLANDS IN VITRO

1981 ◽  
Vol 88 (3) ◽  
pp. 329-338 ◽  
Author(s):  
J. DE KONING ◽  
J. A. M. J. VAN DIETEN ◽  
A. M. I. TIJSSEN ◽  
G. P. VAN REES
Keyword(s):  
Protein Synthesis ◽  
Luteinizing Hormone ◽  
Cyclic Amp ◽  
Female Rats ◽  
Releasing Hormone ◽  
Pituitary Tissue ◽  
Pituitary Glands ◽  
Lh Release ◽  
Lh Rh ◽  
Lh Releasing Hormone

The involvement of cyclic AMP in the action of LH releasing hormone (LH-RH) on LH secretion was studied by incubating pituitary glands from adult female rats on day 2 of dioestrus with 1 mm-N6-monobutyryl cyclic AMP (mbcAMP) and 10 mm-theophylline for periods of up to 10 h. This treatment induced a pattern of LH release similar to that observed in the presence of a low concentration of LH-RH (0·1 ng LH-RH/ml), i.e. an initial 4 h period during which the release of LH was minimal was followed subsequently by an increased rate of release. In this system inhibition of protein synthesis by cycloheximide (25 μg/ml) did not impair the initial response of the pituitary tissue but the increase in the rate of LH release during the second phase of the response was blocked. Preincubation with mbcAMP and theophylline increased the responsiveness of the pituitary tissue to LH-RH. This action could be prevented by including cycloheximide during the preincubation period, whereas addition of this drug during the incubation with LH-RH no longer impaired the increased responsiveness. The size of the sensitizing action of mbcAMP and theophylline mediated through the induction of protein synthesis was comparable with that of a high concentration of LH-RH. From the absence of a significant change in total LH during the preincubation period, it was concluded that the increased responsiveness was not the result of newly synthesized LH. The present results suggest a role or roles for cyclic AMP in the secretion of LH induced by LH-RH. Besides an effect on the formation of a factor related to the synthesis of protein, other than LH which has a permissive role in the acute release of LH, cyclic AMP might also be concerned in the secretion process through a pathway which does not involve synthesis of protein.

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.

Luteinizing hormone responses to repeated injections of luteinizing hormone releasing hormone in the rat during the oestrous cycle and after ovariectomy with or without oestrogen treatment

1982 ◽  
Vol 93 (2) ◽  
pp. 161-168 ◽  
Author(s):  
Takashi Higuchi ◽  
Masazumi Kawakami
Keyword(s):  
Luteinizing Hormone ◽  
Priming Effect ◽  
Oestrous Cycle ◽  
Female Rats ◽  
Oestrogen Treatment ◽  
Releasing Hormone ◽  
First Response ◽  
Serum Lh ◽  
Lh Rh ◽  
Lh Releasing Hormone

In order to characterize the nature of the LH response to exogenous LH releasing hormone (LH-RH) in female rats during the oestrous cycle and after ovariectomy with or without oestrogen treatment, serum LH levels were determined after repeated LH-RH injections (300 ng/kg body wt, six times with 30-min intervals). The LH response to the first LH-RH stimulation was greatest on the days of pro-oestrus and oestrus followed by dioestrus 2 and dioestrus 1. Second and subsequent LH-RH challenges enhanced the LH response only on pro-oestrus and dioestrus 2. Larger doses of LH-RH (3 μg/kg body wt) induced a small self-priming effect on dioestrus 1 and oestrus. The LH response to the first LH-RH administration increased with time up to 30 days after ovariectomy and then reached a plateau. A small self-priming effect was present in rats ovariectomized for 30 and 60 days, but absent in rats ovariectomized for 5, 10 and 120 days. Oestrogen treatment increased the self-priming effect in rats ovariectomized for 5 days, with little sensitization of the pituitary gland to the first LH-RH injection on the next day. In rats ovariectomized for 120 days, oestrogen treatment enhanced responsiveness to the first and successive LH-RH stimulations on the next day, and further enhancement to the first response only was induced 3 days after oestrogen treatment.

EFFECT OF OESTROGEN ON GONADOTROPHIN RELEASE IN STUMPTAILED MONKEYS (MACACA ARCTOIDES) TREATED CHRONICALLY WITH AN AGONIST ANALOGUE OF LUTEINIZING HORMONE RELEASING HORMONE

1981 ◽  
Vol 91 (3) ◽  
pp. 525-530 ◽  
Author(s):  
H. M. FRASER
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Provocation Test ◽  
Significant Rise ◽  
Macaca Arctoides ◽  
Normal Cycle ◽  
Lh Surge ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Lh Rh

Nine adult female stumptailed monkeys (Macaca arctoides) treated chronically with daily s.c. injections of d-Ser(But)6des-Gly10,Proethylamide9, luteinizing hormone releasing hormone (LH-RH agonist) to inhibit ovulation, were tested for their ability to respond to an oestrogen provocation test (positive feedback). On two occasions during treatment with the LH-RH agonist (first test between 10 and 35 weeks after treatment had started; second test between 30 and 60 weeks after) the animals were given an i.m. injection of 50 μg oestradiol benzoate/kg in arachis oil. Controls were tested between days 1 and 5 of the normal cycle. In the control monkeys oestrogen induced a clear rise in LH and FSH concentrations in the blood, with highest values between 48 and 60 h after treatment. In marked contrast, none of the animals treated with LH-RH agonist showed this pattern of response. In the first test, five of the nine monkeys showed no rise in LH while in the remaining animals the response was diminished or delayed, and in the second test all nine failed to show a significant rise in LH. In all agonist-treated monkeys oestrogen failed to cause an FSH rise in either test. Thus, chronic treatment with LH-RH agonist in the monkey either abolishes, diminishes or delays the oestrogen-induced LH surge. Since, in the primate, oestrogen appears to release LH by acting directly on the pituitary gland exposed to pulses of LH-RH from the hypothalamus it appears that the LH surge is inhibited primarily because the pituitary gland has been exposed to prolonged stimulation by the agonist.

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.

RESTORATION OF OESTROGEN POSITIVE FEEDBACK EFFECT ON LH RELEASE BY BROMOCRIPTINE IN HYPERPROLACTINAEMIC PATIENTS WITH GALACTORRHOEA-AMENORRHOEA

1979 ◽  
Vol 91 (3) ◽  
pp. 591-600 ◽  
Author(s):  
Toshihiro Aono ◽  
Akira Miyake ◽  
Takenori Shioji Motoi Yasuda ◽  
Koji Koike ◽  
Keiichi Kurachi
Keyword(s):  
Luteinizing Hormone ◽  
Follicle Stimulating Hormone ◽  
Serum Prolactin ◽  
Serum Luteinizing Hormone ◽  
Serum Lh ◽  
Lh Release ◽  
The Mean ◽  
Lh Rh ◽  
Lh Releasing Hormone ◽  
Positive Feedback Effect

ABSTRACT Five mg of bromocriptine was administered for 3 weeks to 8 hyperprolactinaemic women with galactorrhoea-amernorrhoea, in whom the response of serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) to 100 μg of iv LH-releasing hormone (LH-RH) had been evaluated. Twenty mg of conjugated oestrogen (Premarin®) was injected iv any day between the 10th and 12th day from the initiation of the treatment, and serum LH levels were serially determined for 120 h. Hyperresponse of LH with normal FSH response to LH-RH was observed in most patients. Bromocriptine treatment for 10 to 12 days significantly suppressed mean (± se) serum prolactin (PRL) levels from 65.1 ± 23.0 to 10.4 ± 2.0 ng/ml, while LH (12.6 ± 2.1 to 24.8 ± 5.9 mIU/ml) and oestradiol (40.1 ± 7.6 to 111.4 ± 20.8 pg/ml) levels increased significantly. Patients on bromocriptine treatment showed LH release with a peak at 48 h after the injection of Premarin. The mean per cent increases in LH were significantly higher than those in untreated patients with galactorrhoea-amenorrhoea between 32 and 96 h after the injection. The present results seem to suggest that the restoration of LH-releasing response to oestrogen following suppression of PRL by bromocriptine may play an important role in induction of ovulation in hyperprolactinaemic patients with galactorrhoea-amenorrhoea.

SERUM LUTEINIZING HORMONE AND FOLLICLE-STIMULATING HORMONE CONCENTRATIONS IN IMMATURE FEMALE RATS TREATED WITH MULTIPLE INJECTIONS AND VARIOUS AMOUNTS OF LUTEINIZING HORMONE RELEASING HORMONE

1975 ◽  
Vol 66 (1) ◽  
pp. 13-20 ◽  
Author(s):  
D. C. JOHNSON ◽  
R. S. MALLAMPATI
Keyword(s):  
Luteinizing Hormone ◽  
Constant Stimulus ◽  
Female Rats ◽  
Intact Female ◽  
Immature Female ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Serum Luteinizing Hormone ◽  
Serum Lh ◽  
Lh Rh

SUMMARY Release of immunoreactive LH and FSH was induced in immature intact female rats by repeated injections of synthetic luteinizing hormone releasing hormone (LH-RH). Altering the dose of LH-RH (5, 10, 20, 50 ng) and the frequency of administration (every 10, 20, 30 or 60 min) over a period of 2 h produced a variety of serum LH and FSH concentrations and ratios. When the dose was a constant 20 ng but the frequency of injections was either 20 or 30 min, a steady state in serum gonadotrophin concentrations was reached within 1 h and the level remained the same during the second hour. When given every 10 min, 20 ng LH-RH produced a much higher concentration of both LH and FSH during the second hour of stimulation. Examination of the gonadotrophin levels after each injection of LH-RH showed that the pituitary response was variable in spite of a constant stimulus.

EFFECTS OF MATING AND INJECTION OF LUTEINIZING HORMONE RELEASING HORMONE ON SERUM LUTEINIZING HORMONE AND TESTOSTERONE CONCENTRATIONS IN RABBITS

1978 ◽  
Vol 76 (3) ◽  
pp. 417-425 ◽  
Author(s):  
C. A. BLAKE ◽  
PATRICIA K. BLAKE ◽  
NANCY K. THORNEYCROFT ◽  
I. H. THORNEYCROFT
Keyword(s):  
Luteinizing Hormone ◽  
Serum Testosterone ◽  
Serum Levels ◽  
Transient Increase ◽  
Marked Rise ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Serum Lh ◽  
Before And After ◽  
Lh Rh

The effects of coitus and injection of luteinizing hormone releasing hormone (LH-RH) on serum concentrations of LH, testosterone and dihydrotestosterone (17β-hydroxy-5α-androstan-3-one; DHT) were tested in male rabbits. Before experimentation, male and female rabbits were housed in individual cages in the same room. Male rabbits were then bled by cardiac puncture before and after placement with female rabbits or intravenous injection of LH-RH. Serum LH, testosterone and DHT were measured by radioimmunoassay. Sexual excitement (sniffing, chasing and mounting), with or without intromission, caused a marked rise in serum testosterone and DHT concentrations in only some of the bucks. These increases were accompanied or preceded by a small, transient increase in serum LH. In the rest of the bucks, sexual excitement with or without intromission had either no effect on serum levels of all three hormones, or only serum testosterone and DHT decreased during the collection period. Similar responses were measured in bucks which were housed in a room without does for 2–4 weeks before experimentation. Injection of 10, 30 or 100 ng or 50 μg LH-RH caused serum LH, testosterone and DHT to rise in all bucks tested, but the magnitude of the rises in serum testosterone and DHT were not related to the magnitude of the LH rise. In both mated and LH-RH-injected bucks, the rises in serum testosterone and DHT were greatest in animals with low initial testosterone and DHT values. Under the conditions of this study, the data suggest that: (1) serum testosterone and DHT rise in only some male rabbits after sexual excitement (with or without intromission), (2) the rises in serum testosterone and DHT are dependent on a small transient increase in serum LH and (3) sexual excitement is less likely to cause release of LH-RH in bucks with raised serum testosterone and DHT concentrations.

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