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

Changes in pituitary responsiveness to LH-releasing hormone after acute buserelin treatment: a time-course and dose–response study

1985 ◽  
Vol 106 (1) ◽  
pp. 27-30 ◽  
Author(s):  
J. D. Heather ◽  
S. A. Whitehead
Keyword(s):  
Time Course ◽  
Dependent Manner ◽  
Releasing Hormone ◽  
Serum Lh ◽  
Significant Difference ◽  
Lh Release ◽  
Lh Releasing Hormone ◽  
In Vivo Effects ◽  
Dose Response Study

ABSTRACT The acute in-vivo effects of a potent LH-releasing hormone (LHRH) agonist, buserelin, on LH secretion and pituitary responsiveness to LHRH have been investigated in oestrous rats. Doses of 50, 100 and 250 ng buserelin stimulated LH release in a dose-dependent manner, the peak serum LH concentrations being measured 1 h after the treatment. Thereafter LH levels fell rapidly between 1 and 6 h and by 18 h serum LH concentrations were similar in all groups of animals. Pituitary responsiveness to a challenge with 100 ng LHRH was potentiated by 50 or 100 ng buserelin injected 1 or 2 h before the LHRH challenge. In contrast, 250 ng buserelin completely abolished the LH response to LHRH when tested 1, 2 and 4 h after treatment, but by 6 h a small but attenuated response was observed. Four hours after treatment there was no significant difference in the responses when compared with the saline-treated controls. J. Endocr. (1985) 106, 27–30

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.

TESTOSTERONE AND OESTRADIOL SUPPRESSION OF LH AND FSH IN ADULT MALE RATS: DURATION OF CASTRATION, DURATION OF TREATMENT AND COMBINED TREATMENT

1973 ◽  
Vol 73 (1) ◽  
pp. 11-21 ◽  
Author(s):  
R. S. Swerdloff ◽  
P. C. Walsh
Keyword(s):  
Adult Male ◽  
Testosterone Propionate ◽  
Combined Treatment ◽  
Male Rats ◽  
Low Doses ◽  
Duration Of Treatment ◽  
Serum Lh ◽  
Oestradiol Benzoate ◽  
Hypothalamic Pituitary Axis ◽  
Androgen Effect

ABSTRACT The effects of androgens and oestrogens on serum LH and FSH in castrated rats were evaluated with regard to the modifying influences of duration of castration, duration of treatment and combined oestrogen-androgen effect. Serum LH was not greatly influenced by these variables. In contrast, serum FSH was shown to be more resistant to suppression by both steroids after at least five days of castration, requiring a longer duration of treatment to be suppressed to intact levels. Combined treatment of submaximally suppressive doses of testosterone propionate and oestradiol benzoate resulted in no additive effect on lowering serum FSH. Low doses of both androgens and oestrogens resulted in elevated levels of serum LH and FSH, suggesting that the adult male hypothalamic-pituitary axis may be responsive to positive feedback. In all studies, testosterone preferentially suppressed serum LH as compared to serum FSH. In contrast, oestradiol administration produced parallel inhibition of both LH and FSH. It is emphasized that neither oestrogen nor androgen alone, nor in combination, resulted in preferential inhibition of serum FSH over LH.

Effects of Testosterone Metabolites on Serum Gonadotropin Concentrations in Immature Male Rats

1975 ◽  
Vol 53 (5) ◽  
pp. 839-844 ◽  
Author(s):  
William H. Moger
Keyword(s):  
Body Weight ◽  
Testosterone Propionate ◽  
Male Rats ◽  
Ventral Prostate ◽  
Male Rat ◽  
Control Group ◽  
Immature Male ◽  
Serum Lh ◽  
Serum Gonadotropin ◽  
Testosterone Metabolites

The ability of testosterone, androsterone, 5α-androstane-3α,17β-diol, and 5α-androstane-3β,17β-diol to prevent the castration-induced rise in serum gonadotropin levels was investigated in immature male rats. Rats castrated at 30 days of age were treated once per day by subcutaneous injection of 12.5–100 μg of the steroid per 100 g body weight per day for 3 days, beginning on the day of castration. The animals were sacrificed 24 h after the last injection. Testosterone propionate, androsterone propionate, and 5α-androstane-3α,17β-diol dipropionate were also tested at the approximate molar equivalent of 100 μg of the free alcohol form per 100 g body weight per day.Testosterone propionate and 5α-androstane-3α,17β-diol were the only compounds tested that prevented the castration induced rise in luteinizing hormone (LH) concentrations. Testosterone propionate also inhibited the rise in follicle stimulating hormone (FSH) concentrations whereas 5α-androstane-3α,17β-diol inhibited the rise in FSH in one but not in another experiment. These were the only compounds tested that affected serum FSH concentrations.The lower doses of testosterone tested significantly increased serum LH, but not FSH concentrations compared to castrate control animals. The highest dose tested partially inhibited the rise in serum LH concentrations.Both androsterone and androsterone propionate maintained ventral prostate weights. Although neither compound prevented the castration induced rise in serum LH, two groups receiving androsterone had serum LH concentrations significantly lower than the castrate control group.5α-Androstane-3β,17β-diol and 5α-androstane-3α,17β-diol dipropionate failed to maintain ventral prostate weights or prevent the rise in serum gonadotropin levels.These results indicate that 5α-androstane-3α,17β-diol is capable of preventing the castration induced rise in serum LH concentrations in the immature male rat and thus may participate in the regulation of LH secretion in these animals.

Ontogeny of serum and pituitary gonadotrophins in male rats treated with low doses of 5α-dihydrotestosterone

1986 ◽  
Vol 108 (3) ◽  
pp. 369-375 ◽  
Author(s):  
S. Karanth ◽  
M. K. Gill ◽  
A. Dutt ◽  
N. Lehri ◽  
H. S. Juneja
Keyword(s):  
Body Weight ◽  
Male Rats ◽  
Male Rat ◽  
Low Doses ◽  
Releasing Hormone ◽  
Serum Lh ◽  
Lh Releasing Hormone

ABSTRACT The effect of s.c. daily injections of 10 or 1000 ng 5α-dihydrotestosterone (DHT)/100 g body weight from birth to day 21, or from days 26 to 117 of age, on the changes in concentration of serum and pituitary gonadotrophins was investigated in male rats. Treatment with 10 ng DHT from days 1 to 21 depressed serum FSH, but not LH, at day 7, while 1000 ng DHT depressed both serum LH and FSH. Treatment with both doses of DHT reduced pituitary levels of LH and FSH at day 7, with FSH being more depressed than LH. Treatment with 10 ng DHT from days 26 to 117 increased serum FSH from days 82 to 117, while 1000 ng DHT did not have this effect. Treatment with 1000 ng, but not 10 ng, DHT between days 26 and 117 reduced pituitary levels of LH and FSH at day 40. Rats treated with the two doses of DHT from days 26 to 117 showed a difference in the responsiveness of the pituitary to LH-releasing hormone (LHRH). Treatment with 10 ng DHT enhanced LHRH-induced release of LH without affecting FSH release, while 1000 ng DHT depressed LHRH-induced release of FSH but not of LH. These findings support the view that DHT may play a modulatory role in the ontogeny of serum gonadotrophins and the responsiveness of the pituitary to LHRH during the onset of puberty in the male rat. J. Endocr. (1986) 108, 369–375

EFFECTS OF TESTOSTERONE PROPIONATE, 5α-DIHYDROTESTOSTERONE PROPIONATE AND OESTRADIOL BENZOATE ON SERUM LEVELS OF LH AND FSH IN THE CASTRATED ADULT MALE RAT

1974 ◽  
Vol 77 (4) ◽  
pp. 643-654 ◽  
Author(s):  
H. L. Verjans ◽  
K. B. Eik-Nes ◽  
J. H. Aafjes ◽  
F. J. M. Vels ◽  
H. J. van der Molen
Keyword(s):  
Adult Male ◽  
Testosterone Propionate ◽  
Serum Levels ◽  
Seminal Vesicles ◽  
Male Rats ◽  
Male Rat ◽  
Low Doses ◽  
Serum Lh ◽  
Oestradiol Benzoate ◽  
Adult Male Rat

ABSTRACT The influence of treatment with various doses of testosterone propionate, 5α-dihydrotestosterone propionate or oestradiol benzoate on serum levels of LH and FSH (measured by radioimmunoassay) and on weights of ventral prostates and seminal vesicles was investigated in castrated, adult, male rats. For depression of the high, castrate levels of serum gonadotrophins with either of these steroid esters, the inhibition curves were different for LH and for FSH. Serum LH was kept at levels encountered in intact, adult, male rats by lower doses of steroid ester than was serum FSH. Oestradiol benzoate was the most potent suppressor of the serum gonadotrophins among the steroid esters tested, testosterone propionate the least. Treatment with low doses of oestradiol benzoate, however, resulted in serum FSH levels significantly above those of castrates treated with vehicle only. Finally, administration of a synthetic LH-releasing factor to testosterone propionate, 5α-dihydrotestosterone propionate or oestradiol benzoate treated, castrated, adult, male rats resulted in a further release of both LH and FSH. The latter effect was more pronounced in oestradiol benzoate treated castrates than in testosterone propionate or 5α-dihydrotestosterone propionate treated castrates.

IMMATURE RAT PITUITARY GLANDS IN VITRO: AGE- AND SEX-RELATED CHANGES IN LUTEINIZING HORMONE RELEASING HORMONE-STIMULATED GONADOTROPHIN RELEASE

1977 ◽  
Vol 73 (2) ◽  
pp. 309-319 ◽  
Author(s):  
J. DULLAART
Keyword(s):  
Male Rats ◽  
Steady Increase ◽  
Releasing Hormone ◽  
Rat Pituitary ◽  
Pituitary Glands ◽  
Lh Release ◽  
The One ◽  
Lh Rh ◽  
Lh Releasing Hormone

SUMMARY Pituitary glands from immature female and male rats aged between 5 and 30 days were incubated in vitro and the effect of LH releasing hormone (RH) on the release of LH and FSH was studied. Pituitary gonadotrophin contents were also measured. Gonadotrophin release showed changes with age as well as sex differences: after LH-RH stimulation the female pattern of release of LH and FSH (expressed per mg pituitary tissue) showed a peak at day 15; the male pattern of LH release was characterized by a steady increase with age, whereas FSH release stayed more or less constant from day 10 onwards. In both sexes the LH:FSH ratio increased with age, both in pituitary gonadotrophin content and in the mixture of gonadotrophins released. It is discussed, that the prepubertal development of pituitary gonadotrophic function might be determined on the one hand by rather autonomous growth processes (more or less similar in female and male hypophyses) and on the other hand by modulating influences of sex steroid hormones, which are different in female and male animals.

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.

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.

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