ANAESTHESIA WITH PENTOBARBITONE BLOCKS THE PROGESTERONE-INDUCED LUTEINIZING HORMONE SURGE IN THE OVARIECTOMIZED RHESUS MONKEY

1982 ◽  
Vol 92 (3) ◽  
pp. 327-339 ◽  
Author(s):  
E. TERASAWA ◽  
J. NOONAN ◽  
W. E. BRIDSON
Keyword(s):  
Pituitary Gland ◽  
Peak Latency ◽  
Single Peak ◽  
First Response ◽  
Sequential Administration ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Series Of Experiments ◽  
Lh Releasing Hormone ◽  
A Site

Although the anterior pituitary gland has been shown to be a site of oestrogen feedback in the non-human primate, the role of the hypothalamus as a site of ovarian steroid feedback in facilitating gonadotrophin release has not been ruled out. In the present study, LH release in response to 2·5 mg progesterone with oestradiol benzoate (OB; 10 μg or 30 μg) 30 h earlier was observed in the ovariectomized monkey. Then pentobarbitone sodium was administered to block the progesterone-induced LH response. Serum levels of LH, oestradiol (OE2) and progesterone were measured by radioimmunoassay. In the first series of experiments a group of nine rhesus monkeys received subcutaneous implants of a small silicone elastomer capsule containing OE2. Two weeks later, either OB and oil, or OB and progesterone were injected sequentially. Oestradiol benzoate (10 μg) followed by oil 30 h later failed to cause any clear LH release, while 30 μg OB followed by oil induced a single peak of LH release with a peak latency of 16·5 ± 1·9 (s.e.m.) h after oil, and a duration of 69·8 ± 10·2 h. Regardless of the dose of OB, however, progesterone induced an LH release with two peaks in all animals. The peak latency (7·3 ±0·9 h) and the duration (19·3 ±1·3 h) of the first response with 30 μg OB + progesterone were virtually identical to those with 10 μg OB + progesterone (7·0 ±0·7 h, 18·0 ± 1·4 h respectively), whilst both components of the first response with 30 μg OB + progesterone were significantly shorter than those with 30 μg OB + oil (P < 0·001 for both). The peak latency of the second response with 30 μg OB + progesterone (42·7+ 4·8 h) was similar to that with 10 μg OB + progesterone (38·3 ±3·2 h), but the duration of the second response with 30 μg OB + progesterone (46·0 ± 1·7 h) was longer than that (35·7 ±3·2 h) with 10 μg OB + progesterone (P <0·02). In the second series of experiments the same nine animals received an OE2-capsule implantation and 10 μg OB (subthreshold) injections before pentobarbitone and progesterone. Pentobarbitone was first given 6 h before progesterone and additional injections were made to maintain the anaesthetized state for 21·6 ± 1·3 h. This period was to cover the progesterone-induced first LH response. Pentobarbitone completely blocked the expected first response of the progesterone-induced LH release in six animals. In the remaining three animals an enhanced LH surge occurred, but it consisted of a single peak with long latency 16·0 ± 2·0 h) and duration (66·0 ± 10·5 h) and was essentially the same as that observed in animals treated with a suprathreshold dose (30 μg) of OB alone. Anaesthesia did not, on the other hand, alter the response of the pituitary gland to LH releasing hormone. Therefore it was concluded that (1) sequential administration of oestrogen and progesterone induces an LH release with two phases in the ovariectomized monkey and (2) the facilitatory action of progesterone on the first phase of LH release requires the involvement of the brain.

Pituitary and testicular responses in sexually mature bulls after intravenous injections of graded doses of LH-releasing hormone

1984 ◽  
Vol 103 (3) ◽  
pp. 371-376 ◽  
Author(s):  
M. J. D'Occhio ◽  
B. P. Setchell
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Anterior Pituitary Gland ◽  
Limiting Factor ◽  
Releasing Hormone ◽  
Intravenous Injections ◽  
Gonadotrophin Secretion ◽  
Lh Release ◽  
Lh Releasing Hormone ◽  
Sexually Mature

ABSTRACT The capacity of the anterior pituitary gland and testes in mature bulls (705±9 (s.e.m.) kg body wt, n = 4) to respond to graded doses of LH-releasing hormone (LHRH) was assessed relative to endogenous profiles of LH and testosterone secretion. Endogenous hormone profiles were determined by bleeding bulls at 20-min intervals for 12 h. Responses to LHRH were assessed on successive days after single intravenous injections of 1, 5, 10, 50 or 100 ng LHRH/kg body wt. Blood samples were taken at −40, −20, 0, 10, 20, 30, 40, 60 and 120 min relative to LHRH injection. During a 12-h bleed bulls showed spontaneous pulses of LH and testosterone which had peak amplitudes of 2·6±0·5 μg/l and 44·5 ± 7·1 nmol/l respectively. Respective peak LH (μg/l) and testosterone (nmol/l) responses to LVRH were as follows: 1 ng LHRH (3·0±0·7: 47·3±4·1); 5 ng LHRH (8·0±1·2; 52·8 ± 6·2); 10 ng LHRH (11·1±2·3; 57·7 ± 9·1); 50 ng LHRH (19·2±2·8; 47·9±8·6); 100 ng LHRH (19·1±4·7; 43·9 ±6·4). A dose of 1 ng LHRH/kg produced LH and testosterone responses which were comparable in amplitude to spontaneous peaks in the respective hormone. There was a linear (y = 0·28x+5·72; r = 0·81) increase in the LH response to doses of LVRH between 1 and 50 ng/kg; corresponding testosterone responses showed no relationship with the dose of LHRH. The capacity of the anterior pituitary gland to release amounts of LH eight to ten times in excess of those secreted during spontaneous peaks suggests that (1) there exists a large releasable store of LH in the anterior pituitary gland and (2) hypothalamic LHRH is a limiting factor in gonadotrophin secretion. In contrast to LH release, the androgenic response of the testes to acute gonadotrophic stimulation is determined largely by prevailing steroidogenic activity. J. Endocr. (1984) 103, 371–376

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.

EFFECTS OF AN ANTI-OESTROGEN, TAMOXIFEN (ICI 46,474), ON LUTEINIZING HORMONE RELEASE AND OVULATION IN THE HEN

1981 ◽  
Vol 88 (2) ◽  
pp. 309-316 ◽  
Author(s):  
SUSAN C. WILSON ◽  
F. J. CUNNINGHAM
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Intramuscular Injection ◽  
Hormone Release ◽  
Luteinizing Hormone Release ◽  
Facilitative Role ◽  
Lh Release ◽  
Lh Rh ◽  
Lh Releasing Hormone

The role of oestradiol in the regulation of LH release in the hen was studied by use of the anti-oestrogen, tamoxifen (ICI 46,474). Intramuscular injection of laying hens with 2 or 4 mg tamoxifen on 2 successive days delayed or prevented the occurrence of the preovulatory release of LH and ovulation expected on day 3. Ovulation could be restored by i.v. injection of 20 pg LH releasing hormone (LH-RH). Tamoxifen at a dose of 1 mg affected neither the timing of the preovulatory release of LH nor ovulation. Treatment with 2 or 4 mg tamoxifen on 2 successive days reduced the effectiveness of an i.m. injection of progesterone to stimulate a release of LH. Injection of 1, 2 or 4 mg tamoxifen on 2 successive days significantly raised basal levels of LH in the blood at 24 h after the last injection. This was associated with an increase in the capacity of the pituitary gland to respond to an injection of synthetic LH-RH by a release of LH. These studies suggest that oestradiol has at least two roles in the regulation of LH release in the hen. First, it maintains a low basal level of LH in the blood by reducing the responsiveness of the pituitary gland to LH-RH. Secondly, oestradiol has a facilitative role in the mechanism by which progesterone stimulates the preovulatory release of LH.

Testosterone metabolites do not participate in the control of hypothalamic LH-releasing hormone

1986 ◽  
Vol 109 (2) ◽  
pp. 291-296 ◽  
Author(s):  
M. Zanisi ◽  
F. Celotti ◽  
P. Ferraboschi ◽  
M. Motta
Keyword(s):  
Testosterone Propionate ◽  
Male Rats ◽  
Free Form ◽  
Releasing Hormone ◽  
Specific Radioimmunoassay ◽  
Serum Lh ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Testosterone Metabolites ◽  
Lh Releasing Hormone

ABSTRACT To determine whether the ability of testosterone to increase intrahypothalamic LH-releasing hormone (LHRH) in orchidectomized rats might be explained by the conversion of the hormone into either its 5α-reduced or oestrogenic metabolites, testosterone, 5α-androstan-17β-ol-3-one (DHT), 5α-androstane-3α, 17β-diol (3α-diol) and 5α-androstane-3β,17β-diol (3β-diol) (2 mg/rat per day for 6 days) and oestradiol (0·1, 0·5, 1·0 and 5·0 μg/rat per day for 6 days) were injected into castrated male rats. After 6 days the rats were killed and serum LH levels and intrahypothalamic LHRH stores measured using specific radioimmunoassay procedures. Testosterone and its 5α-reduced metabolites were used in either the free alcohol or the propionate form (dipropionates in the case of the diols); oestradiol was used as oestradiol-17β or in the benzoate form. Treatment with testosterone, DHT, 3α-diol and 3β-diol resulted in a significant decrease in serum LH levels; all the 5α-reduced testosterone derivatives were more effective than testosterone in this respect. Testosterone and DHT propionates suppressed LH release following orchidectomy totally; 3α-diol and 3β-diol dipropionates were less effective. Testosterone increased intrahypothalamic LHRH stores, this effect being much higher after testosterone propionate, i.e. when intrahypothalamic LHRH stores were restored to pre-castration levels. None of the 5α-reduced steroids was capable of modifying the low intrahypothalamic levels of LHRH found following orchidectomy; only 3α-diol dipropionate exhibited some activity, but this was much lower than that of testosterone propionate. Oestradiol-17β was totally ineffective in decreasing serum LH in orchidectomized animals; in contrast, oestradiol benzoate progressively decreased serum LH. Oestradiol in the free form was unable to increase LHRH stores, as was oestradiol benzoate except at the highest dose. The results suggest that the effect exerted by testosterone on hypothalamic LHRH is due to the hormone as such and does not involve its conversion into either 5α-reduced or oestrogenic metabolites. J. Endocr. (1986) 109, 291–296

Monosodium Glutamate and Pituitary Gland Luteinizing Hormone (LH) Release in Response to LH-Releasing Hormone: Anin VitroStudy*

Endocrinology ◽  
1985 ◽  
Vol 116 (1) ◽  
pp. 246-251 ◽  
Author(s):  
M. OLUBUNMI DADA ◽  
JORGE F. RODRIGUEZ-SIERRA ◽  
RICHARD W. CLOUGH ◽  
LAURA L. GARNER ◽  
CHARLES A. BLAKE
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Monosodium Glutamate ◽  
Releasing Hormone ◽  
Lh Release ◽  
Lh Releasing Hormone

Prostaglandin D2 induces release of luteinizing hormone from the rat pituitary gland without the modulation of hypothalamic luteinizing hormone releasing hormone

1983 ◽  
Vol 99 (2) ◽  
pp. 289-292 ◽  
Author(s):  
K. Tasaka ◽  
A. Miyake ◽  
T. Sakumoto ◽  
T. Aono ◽  
K. Kurachi
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Direct Action ◽  
Female Rats ◽  
Prostaglandin D2 ◽  
Medial Basal Hypothalamus ◽  
Releasing Hormone ◽  
In Series ◽  
Lh Release ◽  
Lh Releasing Hormone

The effect of prostaglandin D2 (PGD2) on release of LH and LH releasing hormone (LHRH) was studied in a sequential double-chamber superfusion system using the medial basal hypothalamus (MBH) and the pituitary gland from female rats at dioestrus. Infusion of PGD2 (5·7 or 57μmol/l) caused a significant (P <0·05) increase in LH release to values 40–60% above the preinjection values from the pituitary gland superfused either alone or in series with the MBH. No release of LHRH in response to PGD2 was observed from the superfused MBH. These data demonstrate that PGD2 causes LH release from the pituitary gland not by inducing release of hypothalamic LHRH but by a direct action on the gland.

Recovery of the pituitary gland from LRH-induced refractoriness to LRH in the ovariectomized rat

1981 ◽  
Vol 96 (3) ◽  
pp. 315-320 ◽  
Author(s):  
T. R. Koiter ◽  
N. Pols-Valkhof ◽  
G. A. Schuiling
Keyword(s):  
Pituitary Gland ◽  
Ovariectomized Rats ◽  
Ovariectomized Rat ◽  
Time Intervals ◽  
Absolute Value ◽  
Lh Release ◽  
Series Of Experiments ◽  
Lh Secretion ◽  
Determining Factor ◽  
Stimulation Of

Abstract. Recovery of the pituitary gland from LRH-induced refractoriness to LRH was studied in 5-weeks ovariectomized rats. Rats first received over a period of 48 h an infusion of LRH at a rate of 416 ng/h. After discontinuation of this infusion pituitary LH content had decreased to about 50% of its original value and the rate of LH secretion decreased markedly. Over a period of 72 h after discontinuation of the infusion plasma LH values rose to pre-infusion values but pituitary LH content showed such a recovery only partly. In another series of experiments a second infusion of LRH was given during 24 h and again at a rate of 416 ng/h, starting 3, 12, 24 or 72 h after discontinuation of the first infusion. It induced rises of LH secretion which were smaller than those following the first infusion, indicating refractoriness of the pituitary gland to LRH. However, the LH responses became progressively larger with increasing time intervals after the end of the first infusion. This stimulation of LH release was accompanied by a further decrease of pituitary LH content which was still depressed after the first infusion. Comparison of plasma LH levels and pituitary LH content indicated that pituitary responsiveness to LRH can recover independently from pituitary LH content. It can also be concluded that the absolute value of the blood LRH concentration can not be the sole determining factor of LH secretion.

Influence of the pituitary-adrenal axis on the induced release of luteinizing hormone in rams

1983 ◽  
Vol 99 (1) ◽  
pp. 151-155 ◽  
Author(s):  
J. W. Fuquay ◽  
G. P. Moberg
Keyword(s):  
Luteinizing Hormone ◽  
Adrenal Gland ◽  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Releasing Hormone ◽  
Adrenal Axis ◽  
Acth Treatment ◽  
Lh Release ◽  
Lh Releasing Hormone ◽  
Pituitary Adrenal Axis

Treatment of intact rams with ACTH increased plasma corticosteroids and significantly reduced the ability of LH releasing hormone (LHRH) to elicit the release of LH. Infusion of cortisol at a rate which increased plasma corticosteroid concentrations to above that observed after injection of ACTH did not affect the ability of LHRH to induce the release of LH. In adrenalectomized rams LH release in response to LHRH was inhibited during ACTH treatment but was not affected in the absence of ACTH. Therefore, ACTH reduced the responsiveness of the anterior pituitary gland to LHRH through a mechanism not involving the adrenal gland.

Effect of oestrogen on the responsiveness of the pituitary gland to LRH: the role of corpora lutea

1981 ◽  
Vol 98 (1) ◽  
pp. 29-35
Author(s):  
T. R. Koiter ◽  
N. Pols-Valkhof ◽  
G. A. Schuiling
Keyword(s):  
Pituitary Gland ◽  
Area Under The Curve ◽  
Release Mechanism ◽  
Corpora Lutea ◽  
Constant Rate ◽  
Maximal Height ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Single Set

Abstract. The hypothesis that corpora lutea (CL) secrete substances which prevent oestrogens from influencing the state of responsiveness of the pituitary gland to LRH (RESP) was tested in rats rendered persistently oestrous (PO) by exposure to permanent illumination. In these rats ovulation and hence the presence of a single set of CL, was induced by exogenous gonadotrophin, hCG. The RESP of the animals was judged on 3 parameters based on the surge-like LH-secretory responses which were induced by 21-h long constant rate LRH infusions (104 ng/LRH/h). These 3 parameters were: a) the maximal height (MH) of the responses; b) the 'area under the curve' (AUC) of the LH values; and c) the constant β (or alternatively the t½) which characterizes the rate of decrease of the plasma LH concentrations after 2 h of infusion. Four experiments were performed, all with PO rats: 1) rats were injected with either oestradiol benzoate (OeB; 3 μg sc) or oil on day 0 (the day treatments were started was always denoted as day 0); 2) rats were treated similarly, but they also received an ovulatory dose of hCG (50 IU/100 g b.w. ip) on day 0; 3) rats were injected with hCG on day 0 and with OeB or oil on day 3; and 4) rats were injected with hCG on days 0 and 4, on which latter day they also received OeB or oil. In all 4 experiments the LRH infusions were started 21 h after administration of OeB or oil. Blood samples for LH determinations were taken at times apparent from 'Results and Discussion'. It is observed that: 1) after administration of OeB the MH and thereby the AUC increased significantly but the β of the LH-secretory responses was unchanged; 2) after administration of an ovulatory dose of hCG the LH-secretory responses changed also; of these responses, however, the β had decreased and the AUC had increased, whilst the MH remained unchanged; 3) when given together, OeB and hCG exhibited their effect simultaneously: the two effects are additive; 4) in the presence of 3-day old CL OeB is ineffective; and 5) in the presence of 4-day old CL neither OeB nor hCG is able to affect the RESP. It is concluded: 1) OeB and 'hCG' probably influence a different substrate of the LH-release mechanism; and 2) that these results confirm the hypothesis that CL secrete substances which prevent oestrogen from affecting the RESP for at least 4 days. If this hypothesis is extended to the cyclic rat, CL, arisen after the previous ovulation, may still be of importance on the day of the next pro-oestrus by exerting a significant influence on the RESP.

Reproductive hormone secretion and spermatogenic function in thyroidectomized rams receiving graded doses of exogenous thyroxine

1986 ◽  
Vol 111 (2) ◽  
pp. 245-253 ◽  
Author(s):  
Y. Chandrasekhar ◽  
M. J. D'Occhio ◽  
B. P. Setchell
Keyword(s):  
Hormone Secretion ◽  
Reproductive Function ◽  
Pulse Frequency ◽  
Endocrine Function ◽  
Sex Hormone Binding Globulin ◽  
Testosterone Levels ◽  
Reproductive Endocrine ◽  
Lh Release ◽  
Lh Releasing Hormone ◽  
The Relationship

ABSTRACT This study aimed to obtain a better understanding of the relationship between circulating thyroxine (T4) concentrations and reproductive endocrine function in the ram. Mature Merino rams were thyroidectomized and supplemented with 0, 30, 100 and 300% of normal T4 for 10 weeks. Thyroidectomy had no apparent effect on spermatogenic function but interfered with sperm maturation, the latter being returned to normal by 30% T4 replacement. Circulating testosterone levels were reduced by thyroidectomy and restored to control levels by 30% T4; when T4 levels were supranormal (300%), circulating testosterone levels were again reduced. The lowered circulating testosterone levels in thyroidectomized rams occurred as a result of suppressed testosterone secretion from the testis, observed under basal conditions and also following LH-releasing hormone (LHRH) and human chorionic gonadotrophin injection. In thyroidectomized rams, sex hormone binding globulin (SHBG) levels were depressed without changes in testosterone clearance rate (TCR), while in rams with supranormal T4 levels, TCR was increased without changes in SHBG levels. Subnormal levels of T4 also restored to normal the reduced LH pulse frequency in thyroidectomized rams. Reduced LH pulse frequency, together with diminished LH release following LHRH injection in thyroidectomized rams, suggested effects of T4 at the hypothalamo-pituitary axis. The present study demonstrates that complete lack of thyroid hormones suppresses normal reproductive endocrine function in the ram, but that this can be restored to normal by 30% T4 replacement. The results support the theory that T4 plays a permissive rather than a regulatory role in reproductive function in males. J. Endocr. (1986) 111, 245–253

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