Dynamic changes in plasma luteinizing hormone and testosterone after stress in the male rat. Influence of adrenalectomy

1984 ◽  
Vol 62 (9) ◽  
pp. 1231-1233 ◽  
Author(s):  
Gérard Lescoat ◽  
Denise Lescoat ◽  
Danièle Garnier
Keyword(s):  
Luteinizing Hormone ◽  
Plasma Level ◽  
Male Rats ◽  
Male Rat ◽  
Plasma Testosterone ◽  
Intact Male ◽  
Dynamic Changes ◽  
High Level ◽  
Adrenalectomized Rats ◽  
Stimulation Of

In 60-day old intact male rats, stress imposed by a strange environment increased the levels of plasma LH and testosterone. Adrenalectomy, performed at 50 days of age, decreased plasma level of testosterone in basal conditions. However, without affecting the plasma level of LH significantly, stress increased plasma testosterone, albeit to a lesser extent, in the adrenalectomized rats. Stimulation of the testicular secretion by the high level of ACTH seems to be the most likely explanation for the observed testosterone peak in the adrenalectomized rat.

STUDIES ON THE MECHANISM OF ACTION OF OESTROGENS ON THE PITUITARY-ADRENAL FUNCTION IN THE MALE RAT

1971 ◽  
Vol 68 (4) ◽  
pp. 737-748
Author(s):  
Torsten Perklev
Keyword(s):  
Plasma Corticosterone ◽  
Significant Rise ◽  
Male Rats ◽  
Adrenal Weight ◽  
Male Rat ◽  
Plasma Testosterone ◽  
Intact Male ◽  
Corticosterone Concentration ◽  
Corticosteroid Binding Globulin ◽  
Long Acting

ABSTRACT A single injection of a long-acting oestrogen, polydiethylstilboestrol phosphate (PSP; 200 μg/100 g body weight), into adult male rats caused an enlargement of the adrenal glands and an approximate doubling of total adrenal 3β-hydroxysteroid dehydrogenase (3β-OHD) activity and plasma corticosterone concentration in animals sacrificed 11 to 14 days following injection. The administration of interstitial cell stimulating hormone (ICSH) of human origin or a long-acting testosterone ester (Andradurin®) into the PSP-treated animals partially or completely counteracted the effects of the PSP treatment on adrenal weight and 3β-OHD activity. Daily injections of corticotrophin (ACTH) into intact male rats for 7 days caused a significant rise in the adrenal 3β-OHD activity. Gonadectomy of male rats resulted in increased adrenal weights and elevated adrenal 3β-OHD activity. The plasma corticosterone concentration was unaffected. PSP treatment significantly augmented the effects of the gonadectomy on the adrenal weight and 3β-OHD activity and caused an elevated plasma corticosteroid concentration. The adrenal enlargement following gonadectomy was completely reversed by testosterone replacement but was not influenced by daily injections of ICSH. The data are interpreted as suggesting that the oestrogen-induced hyper-secretion of ACTH in the male rat may be mediated through an elevated activity of the corticosteroid-binding globulin, caused by a reduced plasma testosterone level and a stimulated thyroid activity.

Effects of oestradiol benzoate (OeB) and human chorionic gonadotrophin (hCG) on the testes and accessory sex glands of the rat

1981 ◽  
Vol 96 (2) ◽  
pp. 273-280 ◽  
Author(s):  
Mridula Chowdhury ◽  
Robert Tcholakian ◽  
Emil Steinberger
Keyword(s):  
Treated Group ◽  
Inhibitory Effect ◽  
Male Rats ◽  
Plasma Testosterone ◽  
Control Group ◽  
Intact Male ◽  
Intact Control ◽  
Testosterone Levels ◽  
Oestradiol Benzoate ◽  
Direct Inhibitory Effect

Abstract. It has been suggested that treatment of intact male rats with oestradiol benzoate (OeB) causes an interference with testosterone (T) production by the testes by a direct inhibitory effect on steroidogenesis. To test this hypothesis, different doses (5, 10 or 25 IU) of hCG were administered concomitantly with 50 μg of OeB to adult intact or hypophysectomized male rats. The testicular and plasma testosterone, and serum hCG levels were determined. The sex accessory weights were recorded. In the intact OeB-treated group of animals, hCG stimulated both the secondary sex organs and plasma testosterone levels above the intact control group. However, in hypophysectomized animals, although plasma testosterone levels increased above that of intact controls, their secondary sex organ weights did not. Moreover, inspite of high circulating hCG levels, the testicular testosterone content and concentration remained suppressed in OeB-treated animals. The reason for such dichotomy of hCG action on OeB-treated animals is not clear at present.

Plasma testosterone surge and luteinizing hormone beta (LH-β) following parturition: lack of association in the male rat

1995 ◽  
Vol 133 (3) ◽  
pp. 366-374 ◽  
Author(s):  
Robert F McGivern ◽  
Ralph HM Hermans ◽  
Robert J Handa ◽  
Lawrence D Longo
Keyword(s):  
Luteinizing Hormone ◽  
Cesarean Section ◽  
Gnrh Antagonist ◽  
Male Rat ◽  
Plasma Testosterone ◽  
Treatment Groups ◽  
Natural Birth ◽  
Males And Females ◽  
Lh Secretion

McGivern RF, Hermans RHM, Handa RJ, Longo LD. Plasma testosterone surge and luteinizing hormone beta (LH-β) following parturition: lack of association in the male rat. Eur J Endocrinol 1995; 133:366–74. ISSN 0804–4643 Studies examining the role of luteinizing hormone (LH) in the initiation of the postnatal surge of testosterone in the male rat have produced ambiguous results. We examined the pattern of postnatal LH secretion in the newborn male rat, coincident with plasma testosterone levels, using a specific monoclonal antibody for LH-β. In some males, we attempted to block LH secretion and the postnatal testosterone surge by injecting males with a gonadotropin-releasing hormone (GnRH) antagonist, an LH antibody or progesterone immediately after delivery by cesarean section on day 22. Following injection, animals were immediately sacrificed (time 0) or housed in a humidified incubator maintained at 30°C until sacrifice at 60, 120, 240, 360 or 480 min after delivery. Plasma from individual animals was measured subsequently for LH-β and testosterone by radioimmunoassay. Results revealed a postnatal surge of testosterone which peaked at 2 h after delivery in males from all treatment groups. This testosterone surge was not accompanied by a postnatal rise in plasma LH-β in any group. Administration of the GnRH antagonist or the ethanol vehicle produced a transient drop of approximately 25% in LH-β levels at 60 min but did not decrease the postnatal testosterone surge in the same animals. Additional studies in untreated males and females born by cesarean section or natural birth also failed to reveal a postnatal rise in plasma LH-β during the first 3 h after birth. Plasma levels in both sexes were significantly lower in animals delivered by cesarean section compared to natural birth. Overall, these results indicate that the postnatal surge of testosterone occurs without a corresponding surge of detectable LH-β in the male rat. Robert F McGivern, 6363 Alvarado Ct, Suite 200H. San Diego, CA 92120, USA

SHORT-TERM EFFECTS OF COPULATION, HUMAN CHORIONIC GONADOTROPHIN INJECTION AND NON-TACTILE ASSOCIATION WITH A FEMALE ON TESTOSTERONE LEVELS IN THE MALE RAT

1974 ◽  
Vol 60 (3) ◽  
pp. 429-439 ◽  
Author(s):  
K. PURVIS ◽  
N. B. HAYNES
Keyword(s):  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Physical Contact ◽  
Male Rats ◽  
Male Rat ◽  
Plasma Testosterone ◽  
Short Term ◽  
Testosterone Levels ◽  
Peripheral Plasma ◽  
First Contact

SUMMARY Peripheral plasma testosterone levels in the male rat were increased above control levels 5 min after the first intromission with an oestrous female, or 8–10 min after first contact with the female. The levels remained raised for at least 30 min if copulation was allowed to continue. Intravenous injection of human chorionic gonadotrophin resulted in an increased peripheral concentration of plasma testosterone after 10–15 min and an increase of testosterone content of the testis 5–10 min after injection, indicating that the rat testis has a potential to respond rapidly to gonadotrophin. The results suggested that if the testosterone surge during copulation was gonadotrophin-dependent, it was initiated before the first intromission. Indeed, plasma testosterone levels were raised in male rats 5 min after being placed in the proximity of oestrous females but not allowed physical contact.

Somatostatin Inhibits prolactin secretion in the estradiol primed male rat

1981 ◽  
Vol 59 (10) ◽  
pp. 1082-1088 ◽  
Author(s):  
G. R. Cooper ◽  
S. H. Shin
Keyword(s):  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Blocking Agent ◽  
Prolactin Secretion ◽  
Male Rats ◽  
Male Rat ◽  
Dependent Manner ◽  
Intact Male ◽  
Plasma Prl

Somatostatin inhibits not only growth hormone secretion, but also the secretion of several other hormones. The role of somatostatin in prolactin (PRL) secretion has not been clearly demonstrated. The present study was undertaken to examine the effects of somatostatin on rat PRL secretion in several different circumstances where the circulating PRL level is elevated: (1) the estradiol primed intact male rat, (2) normal and (3) estradiol primed rats pretreated with pimozide, (4) normal and (5) estradiol primed hypophysectomized male rats with adenohypophyses grafted under the kidney capsule (HAG rat). Blood samples (70 μL) were taken every 2 min via an indwelling atrial cannula from conscious, unrestrained animals. In the estradiol primed intact rats, a bolus injection of somatostatin (10, 100, and 1000 μg/kg) lowered PRL levels in a dose-dependent manner. When the PRL concentration was elevated by the administration of pimozide (3 mg/kg), a dopaminergic receptor blocking agent, somatostatin was ineffective in decreasing plasma PRL concentration but the PRL concentration was lowered by somatostatin when the rat had been primed with estradiol. Somatostatin had no effect on the normal HAG rats, but lowered the plasma PRL concentration in the estradiol primed HAG rats. Since somatostatin inhibits PRL secretion only in the estradiol primed rats, it is suggested that estradiol priming creates a new environment, presumably via new or altered receptors, which can be inhibited by somatostatin.

EFFECTS OF FOLLICLE-STIMULATING HORMONE AND LUTEINIZING HORMONE ON PLASMA TESTOSTERONE LEVELS IN HYPOPHYSECTOMIZED AND IN INTACT IMMATURE AND ADULT MALE RATS

1974 ◽  
Vol 61 (2) ◽  
pp. 193-198 ◽  
Author(s):  
S. EL SAFOURY ◽  
A. BARTKE
Keyword(s):  
Luteinizing Hormone ◽  
Adult Male ◽  
Follicle Stimulating Hormone ◽  
Seminal Vesicles ◽  
Male Rats ◽  
Plasma Testosterone ◽  
Adult Rats ◽  
Testosterone Levels ◽  
Hypophysectomized Rats ◽  
Stimulating Hormone

SUMMARY The effects of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) on plasma testosterone levels were examined in hypophysectomized and in intact immature and adult male rats. The animals were injected with saline, LH, FSH, or both gonadotrophins twice daily for 3·5 days and were killed 3 h after the last injection. Plasma testosterone levels were measured by radioimmunoassay. In immature hypophysectomized rats, plasma testosterone levels were not changed by treatment with LH, FSH or LH plus FSH. The weight of the testes and of the seminal vesicles was increased only in animals injected with both LH and FSH. In adult hypophysectomized rats, LH caused the expected increase in plasma testosterone levels, while FSH injected alone had no effect. Plasma testosterone levels in rats treated with 5 μg LH and 20 μg FSH were significantly greater than those in animals given 5 μg LH alone. However, the same dose of FSH did not potentiate the action of 25 μg LH on plasma testosterone levels. In adult hypophysectomized rats the weight of testes was not affected by any of the treatments. The weight of the seminal vesicles was increased by the higher dose of LH and addition of FSH caused no further increase. In intact immature and adult rats plasma testosterone levels and the weight of testes were not changed by any of the treatments. Seminal vesicle weight was increased only in adult rats treated with the higher dose of LH together with FSH. The results demonstrate that FSH potentiates the action of low doses of LH on plasma testosterone levels in adult hypophysectomized rats and suggest that FSH may be involved in the regulation of androgen secretion by the rat testis.

scholarly journals Testosterone-dependent variations in plasma and intrapituitary corticosteroid binding globulin and stress hypothalamic-pituitary-adrenal activity in the male rat

2004 ◽  
Vol 181 (2) ◽  
pp. 223-231 ◽  
Author(s):  
V Viau ◽  
MJ Meaney
Keyword(s):  
Feedback Regulation ◽  
High Plasma ◽  
Male Rats ◽  
Testosterone Replacement ◽  
Male Rat ◽  
Plasma Testosterone ◽  
Hypothalamic Pituitary Adrenal ◽  
Corticosteroid Binding Globulin ◽  
Low Testosterone

Hypothalamic-pituitary-adrenal (HPA) activity is governed by glucocorticoid negative feedback and the magnitude of this signal is determined, in part, by variations in plasma corticosteroid-binding globulin (CBG) capacity. Here, in gonadectomized male rats we examine the extent to which different testosterone replacement levels impact on CBG and HPA function. Compared with gonadectomized rats with low testosterone replacement ( approximately 2 ng/ml), plasma adrenocorticotropin and beta-endorphin/beta-lipotropin responses to restraint stress were reduced in gonadectomized rats with high testosterone replacement ( approximately 5 ng/ml). Plasma CBG levels also varied negatively as a function of testosterone concentration. Moreover, glucocorticoid receptor binding in the liver was elevated by higher testosterone replacement, suggesting that testosterone acts to enhance glucocorticoid suppression of CBG synthesis. Since pituitary intracellular CBG (or transcortin) is derived from plasma, this prompted us to examine whether transcortin binding was similarly responsive to different testosterone replacement levels. Transcortin binding was lower in gonadectomized rats with high plasma testosterone replacement ( approximately 7 ng/ml) than in gonadectomized rats with low testosterone replacement ( approximately 2 ng/ml). This testosterone-dependent decrease in pituitary transcortin was associated, in vitro, with an enhanced nuclear uptake of corticosterone. These findings indicate that the inhibitory effects of testosterone on corticotrope responses to stress may be linked to decrements in plasma and intrapituitary CBG. This could permit greater access of corticosterone to its receptors and enhance glucocorticoid feedback regulation of ACTH release and/or proopiomelanocortin processing.

LEVELS OF LUTEINIZING HORMONE, FOLLICLE-STIMULATING HORMONE, TESTOSTERONE AND DIHYDROTESTOSTERONE IN THE CIRCULATION OF SEXUALLY MATURING INTACT MALE RATS AND AFTER ORCHIDECTOMY AND EXPERIMENTAL BILATERAL CRYPTORCHIDISM

1975 ◽  
Vol 66 (2) ◽  
pp. 183-193 ◽  
Author(s):  
D. GUPTA ◽  
K. RAGER ◽  
J. ZARZYCKI ◽  
M. EICHNER
Keyword(s):  
Plasma Levels ◽  
Follicle Stimulating Hormone ◽  
Plasma Concentrations ◽  
Gonadal Steroids ◽  
Male Rats ◽  
Plasma Testosterone ◽  
Dynamic Feedback ◽  
Gonadal Steroid ◽  
Intact Male ◽  
Bilateral Cryptorchidism

SUMMARY Plasma concentrations of LH, FSH, testosterone and dihydrotestosterone (DHT) have been measured in normal sexually maturing male rats from the age of 16–90 days. Between 16 and 25 days plasma testosterone levels were low, but rose suddenly on day 26. A similar increment occurred at the same time in plasma DHT levels, but this steroid reached its peak concentration later than testosterone. Plasma LH levels rose steadily from day 25 onwards, reaching their highest values on day 30. A marked increase in FSH levels was found on day 16, and a peak was reached on day 33 followed by a decline to a level characteristic of the adult. In addition, plasma levels of all these hormones were estimated in the male animals at various stages of development after orchidectomy and cryptorchidism. Four days after operation, the plasma levels of LH and FSH in the orchidectomized animals reached higher levels than those found in the intact animals, indicating the existence of a dynamic feedback relationship before puberty between gonadal steroids and pituitary gonadotrophic secretion. However, results from the experimental bilaterally cryptorchid animals, suggested that the gonadal steroid–gonadotrophic feedback relationship could not be the only factor initiating puberty.

EFFECTS OF ANTI-OESTROGEN TREATMENT OF NEONATAL MALE RATS ON LORDOSIS BEHAVIOUR AND MOUNTING BEHAVIOUR IN THE ADULT

1978 ◽  
Vol 76 (2) ◽  
pp. 241-249 ◽  
Author(s):  
P. SÖDERSTEN
Keyword(s):  
Testosterone Propionate ◽  
Neonatal Rat ◽  
Male Rats ◽  
Glans Penis ◽  
Male Rat ◽  
Plasma Testosterone ◽  
Oestrogen Treatment ◽  
Oestradiol Benzoate ◽  
Sexual Glands ◽  
Lordosis Behaviour

Male rats were treated daily with 100 μg of the anti-oestrogen ethamoxytriphetol (MER-25) or oil during the first 10 days of life and tested for lordosis behaviour and mounting behaviour as intact adults, after castration and after castration and oestradiol benzoate or testosterone propionate treatment. The MER-25-treated rats showed higher levels of lordosis behaviour than oil-treated rats in all four treatment groups. Under each of these endocrine conditions, except after castration alone, the MER-25-treated rats showed a reduced capacity to ejaculate. Treatment of the neonatal rat with MER-25 reduced body weight in adulthood but did not change the weight of the accessory sexual glands, the testes, the number of cornified papillae on the glans penis or plasma testosterone concentrations during development. The response of the accessory sexual glands and cornified papillae on the glans penis to treatment with oestradiol benzoate or testosterone propionate after castration in adulthood was unaffected by treatment with MER-25. It is suggested that formation of oestrogen in the neonatal male rat brain from testosterone in the circulation inhibits the capacity to show lordosis behaviour and facilitates the capacity to ejaculate in response to gonadal hormone treatment in adulthood.

The contribution of corticosterone and testosterone to the suppression of serum LH in hyperprolactinaemic adult male rats with pituitary transplants

1987 ◽  
Vol 113 (1) ◽  
pp. 111-116 ◽  
Author(s):  
R. F. A. Weber ◽  
M. P. Ooms ◽  
J. T. M. Vreeburg
Keyword(s):  
Adult Male ◽  
Serum Testosterone ◽  
Serum Levels ◽  
Male Rats ◽  
Male Rat ◽  
Serum Concentrations ◽  
Testosterone Secretion ◽  
Accessory Sex Glands ◽  
Serum Lh ◽  
Stimulation Of

ABSTRACT The effects of hyperprolactinaemia on serum levels of LH were investigated in adult male rats of the R × U strain. Hyperprolactinaemia was induced by three pituitary grafts under the kidney capsule, transplanted on day 0 of each experiment. Special attention was paid to the contribution of prolactin-stimulated testes, adrenals and corticosterone. In experiment 1, hyperprolactinaemia significantly reduced the serum concentrations of LH in intact rats. In spite of a significant increase in the serum levels of corticosterone, serum testosterone was not significantly affected by hyperprolactinaemia. The weights of both the adrenals and accessory sex glands were significantly increased at autopsy. In experiment 2, treatment with 10 mg corticosterone s.c. daily from day 14 to day 28 after pituitary grafting significantly reduced serum levels of both LH and testosterone. The suppression of testosterone in the hyperprolactinaemic corticosterone-treated animals was significantly less than in the corticosterone-treated control animals. The weights of the accessory sex glands were significantly increased in the hyperprolactinaemic animals. In experiment 3, rats were adrenalectomized and half of them were substituted with corticosterone. Serum testosterone levels significantly increased in both hyperprolactinaemic adrenalectomized rats and in adrenalectomized corticosterone-treated animals without any significant effect on serum LH. Again the weights of the accessory sex glands were significantly increased in the hyperprolactinaemic animals. In experiment 4, rats were adrenalectomized, gonadectomized and corticosterone treated on day 0 and then implanted with a 2, 1·5 or 1 cm silicone elastomer capsule containing testosterone. On day 28 after pituitary grafting, LH levels were significantly suppressed in animals with a 2 or 1·5 cm testosterone implant. The weights of the accessory sex glands were not increased in the hyperprolactinaemic animals. These results show that in the male rat the inhibitory effects of hyperprolactinaemia on serum LH levels may be due to (1) increased sensitivity of the hypothalamic-pituitary axis to the negative feedback action of testosterone by prolactin and by the prolactin-stimulated corticosterone secretion and (2) stimulation of testicular testosterone secretion by prolactin, which can also explain the increased weights of the accessory sex glands. Even in the presence of high serum concentrations of corticosterone, stimulation of testicular testosterone secretion by prolactin was observed. J. Endocr. (1987) 113,111–116

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