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

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.

1990 ◽  
Vol 258 (1) ◽  
pp. E65-E70 ◽  
Author(s):  
A. R. Gwosdow ◽  
M. S. Kumar ◽  
H. H. Bode

The effect of varying doses of purified human interleukin 1 (IL-1) on rectal temperature (Tr), hypothalamic corticotropin-releasing hormone (CRH), pituitary and plasma adrenocorticotropic hormone (ACTH), and plamsa corticosterone was examined in intact male rats at 24 degrees C; plasma ACTH and corticosterone responses were also studied in hypophysectomized rats. In addition, IL-1-induced changes in corticosterone concentration were investigated by means of adrenal organ cultures. Tr was measured with thermocouples. CRH and ACTH levels were determined by radioimmunoassay, and corticosterone by protein-binding assay. Intravenous administration of IL-1 (0.063-1.0 ng) resulted in hyperthermia, which began 20 min postinjection and continued for an additional 30 min. IL-1 at a dose of 0.5 ng resulted in no change in hypothalamic CRH, pituitary ACTH, or plasma ACTH levels compared with saline-treated rats. Plasma corticosterone was significantly (P less than 0.05) elevated 30 min after IL-1 administration and returned to control levels after 1 h. The higher dose of IL-1 (1.0 ng) did not affect hypothalamic CRH content, but pituitary ACTH began to rise at 15 min and was significantly (P less than 0.05) elevated 30 min after injection. Rats receiving this dose displayed elevated (P less than 0.05) plasma ACTH and corticosterone levels 30 and 60 min postinjection. No change in plasma corticosterone was observed in hypophysectomized rats administered either 1 ng of IL-1 or 1 microgram of recombinant IL-1 beta (rIL-1 beta); adrenal organ cultures treated with IL-1 (10(-11) M) responded similarly.(ABSTRACT TRUNCATED AT 250 WORDS)


2004 ◽  
Vol 181 (2) ◽  
pp. 223-231 ◽  
Author(s):  
V Viau ◽  
MJ Meaney

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.


1984 ◽  
Vol 62 (9) ◽  
pp. 1231-1233 ◽  
Author(s):  
Gérard Lescoat ◽  
Denise Lescoat ◽  
Danièle Garnier

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.


1981 ◽  
Vol 96 (2) ◽  
pp. 273-280 ◽  
Author(s):  
Mridula Chowdhury ◽  
Robert Tcholakian ◽  
Emil Steinberger

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.


2004 ◽  
Vol 181 (2) ◽  
pp. 291-296 ◽  
Author(s):  
J Lesage ◽  
F Del-Favero ◽  
M Leonhardt ◽  
H Louvart ◽  
S Maccari ◽  
...  

There is growing evidence that prenatal adversities could be implicated in foetal programming of adult chronic diseases. Since maternal stress is known to disturb the foetal glucocorticoid environment, we examined the consequences of prenatal stress on foetal growth, on glucose-insulin metabolism and on feeding behaviour in the aged male rat. In foetuses at term, maternal stress reduced body, adrenal and pancreas weight as well as plasma corticosterone and glucose levels. In aged male rats (24 months of age), prenatal stress induced hyperglycaemia and glucose intolerance and decreased basal leptin levels. Moreover, after a fasting period, they showed an increased food intake. These data suggest that maternal stress induces a long-lasting disturbance in feeding behaviour and dysfunctions related to type 2 diabetes mellitus. This programming could be linked to the early restricted foetal growth and to the adverse glucocorticoid environment in utero.


1974 ◽  
Vol 60 (3) ◽  
pp. 429-439 ◽  
Author(s):  
K. PURVIS ◽  
N. B. HAYNES

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.


1981 ◽  
Vol 59 (10) ◽  
pp. 1082-1088 ◽  
Author(s):  
G. R. Cooper ◽  
S. H. Shin

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.


Endocrinology ◽  
2008 ◽  
Vol 149 (7) ◽  
pp. 3244-3253 ◽  
Author(s):  
Susanne K. Droste ◽  
Lotte de Groote ◽  
Helen C. Atkinson ◽  
Stafford L. Lightman ◽  
Johannes M. H. M. Reul ◽  
...  

Circulating corticosterone levels show an ultradian rhythm resulting from the pulsatile release of glucocorticoid hormone by the adrenal cortex. Because the pattern of hormone availability to corticosteroid receptors is of functional significance, it is important to determine whether there is also a pulsatile pattern of corticosterone concentration within target tissues such as the brain. Furthermore, it is unclear whether measurements of plasma corticosterone levels accurately reflect corticosterone levels in the brain. Given that the hippocampus is a principal site of glucocorticoid action, we investigated in male rats hippocampal extracellular corticosterone concentrations under baseline and stress conditions using rapid-sampling in vivo microdialysis. We found that hippocampal extracellular corticosterone concentrations show a distinct circadian and ultradian rhythm. The PULSAR algorithm revealed that the pulse frequency of hippocampal corticosterone is 1.03 ± 0.07 pulses/h between 0900 and 1500 h and is significantly higher between 1500 and 2100 h (1.31 ± 0.05). The hippocampal corticosterone response to stress is stressor dependent but resumes a normal ultradian pattern rapidly after the termination of the stress response. Similar observations were made in the caudate putamen. Importantly, simultaneous measurements of plasma and hippocampal glucocorticoid levels showed that under stress conditions corticosterone in the brain peaks 20 min later than in plasma but clears concurrently, resulting in a smaller exposure of the brain to stress-induced hormone than would be predicted by plasma hormone concentrations. These data are the first to demonstrate that the ultradian rhythm of corticosterone is maintained over the blood-brain barrier and that tissue responses cannot be reliably predicted from the measurement of plasma corticosterone levels.


1975 ◽  
Vol 66 (2) ◽  
pp. 183-193 ◽  
Author(s):  
D. GUPTA ◽  
K. RAGER ◽  
J. ZARZYCKI ◽  
M. EICHNER

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.


2020 ◽  
Vol 10 ◽  
Author(s):  
Neveen Asmet Farag ◽  
Ayman S Mohamed ◽  
Hanan Farag El Sayed ◽  
Eman Y. Salah EL-Din ◽  
Abdel Rahman A. Tawfik

Background:: Infertility is the first-rate public health trouble affecting one in five married couples globally, male causes embody a significant proportion. Natural products could be an alternative or complementary inexpensive treatment for such matters. Echinochrome (Ech) is a natural quinone pigment obtained from sea urchin, and it was confirmed to possess many pharmacological properties due to its chemical activity. Objective:: The current research paper was targeted to evaluate the potential effects of Ech on male fertility, and to highlight the possible involved mechanisms. Methods:: Eighteen adult male rats were randomly distributed into three groups: control (1 ml of 2% DMSO, p.o.), low dose Ech (0.1 mg/kg, p.o.), and high dose Ech (1 mg/kg p.o.). Results:: The high dose Ech caused a significant decline in the levels of glucose, ALT, AST, ALP, urea, Cr, uric acid, TG, TC and LDL-C and testicular tissue MDA, while it caused a significant rise in the levels of albumin, TP, HDL-C, FSH, LH, testosterone and testicular tissue GSH activity. Moreover, it showed a significant positive effect on the testis weight, caudal epididymis weight, sperm count, sperm motility, sperm morphology, fructose concentration, and α-glucosidase activity. However, no significant changes were observed in histological examination of testicular tissue among all groups. Conclusion:: High dose Ech improved male rat-fertility either directly by activating the pituitary gonadal axis, and or indirectly via enhancing: the renal and hepatic functions, the lipid profile and or the antioxidant pathways.


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