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

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.

1985 ◽  
Vol 106 (3) ◽  
pp. 395-NP ◽  
Author(s):  
T. K. Das ◽  
R. Mazumder ◽  
N. M. Biswas

ABSTRACT Quantitative evaluation of spermatogenesis at stage VII of the cycle of the seminiferous epithelium and radioimmunoassay of plasma testosterone were performed in adult Wistar rats after intraventricular injection of 5,6-dihydroxytryptamine (5,6-DHT). The rats were killed 2, 10 and 21 days after injection. Brain 5-hydroxytryptamine (5-HT) and plasma testosterone levels were found to be significantly lower in all rats treated with 5,6-DHT. A significant reduction in step 7 spermatid count was also observed after 10 and 21 days. Supplementation with human chorionic gonadotrophin for 21 days in rats injected with 5,6-DHT partially prevented the step 7 spermatid degeneration and increased testosterone levels without producing any effect on brain concentrations of 5-HT. These results suggest that changes in testicular steroidogenesis and spermatogenesis are secondary to pituitary gonadotrophin release which, in turn, is under the influence of brain 5-HT neurones. J. Endocr. (1985) 106, 395–400


1978 ◽  
Vol 89 (1) ◽  
pp. 126-131 ◽  
Author(s):  
G. Schaison ◽  
F. Durand ◽  
I. Mowszowicz

ABSTRACT ACTH decreases plasma testosterone levels in men. The aim of this study was to assess the part played by the glucocorticoids in this effect, and the mechanism of their action. Plasma androstenedione, testosterone, cortisol and LH were measured in 8 normal men, before and after the following tests: ACTH stimulation (2 mg im), metyrapone administration (500 mg/every 4 h/6 times) and dexamethasone suppression (8 mg/day/3 days). In addition, androstenedione and testosterone were evaluated under human chorionic gonadotrophin (5000 IU HCG/day/3 days) before and after dexamethasone suppression (8 mg/day/6 days). In all patients, ACTH decreased plasma testosterone from 5.87 ± 1.59 (sd) ng/ml to 3.06 ± 0.8 (sd) ng/ml (P < 0.001). In contrast, after metyrapone, the mean plasma testosterone was increased to 6.98 ± 1.75 (sd) ng/ml. This increase, though not statistically significant, was observed in all patients but one. Both tests resulted in a significant increase of plasma androstenedione (P < 0.01 and P < 0.001, respectively). Dexamethasone suppressed both testosterone and androstenedione levels. None of the three tests had a significant effect on the LH concentration. HCG injection increased the mean plasma testosterone to 11.46 ± 2.80 ng/ml. Dexamethasone significantly depressed (P < 0.01) the testosterone response to HCG. These data are consistent with the following conclusions: 1) The decrease of plasma testosterone levels, observed in men after ACTH administration, is not observed after metyrapone induced ACTH increase. This confirms that it is related to cortisol levels rather than to ACTH itself. 2) Glucocorticoids act directly on testicular biosynthesis since they do not induce any change in LH secretion and since dexamethasone reduces testosterone response to HCG.


1973 ◽  
Vol 57 (2) ◽  
pp. 277-284 ◽  
Author(s):  
F. H. DE JONG ◽  
A. H. HEY ◽  
H. J. van der MOLEN

SUMMARY Concentrations of oestradiol-17β and testosterone were estimated in peripheral venous plasma and testicular venous plasma of adult male rats before and after administration of human chorionic gonadotrophin (HCG) or follicle-stimulating hormone (FSH). The concentration of oestradiol-17β in peripheral plasma, as measured with a radioimmunological technique, was 2·0 ± 0·9 (s.d.) pg/ml (n = 12). Peripheral testosterone concentrations were 2·4 ± 1·8 (s.d.) ng/ml (n = 21). Concentrations of oestradiol-17β and testosterone in testicular venous plasma were significantly higher than those in peripheral plasma. After intravenous administration of HCG (100 i.u.), oestradiol-17β and testosterone concentrations in testicular venous plasma increased significantly. After prolonged s.c. administration of HCG (5 days) the concentration of oestradiol-17β in testicular venous plasma did not change significantly, although the concentration of testosterone increased more than ten times. Intravenous administration of HCG after 5 days of pretreatment with HCG caused a significant increase in oestradiol-17β concentrations in testicular venous plasma. The increase in testosterone concentration was not significant under these conditions. Intravenous administration of FSH did not change oestradiol-17β or testosterone concentrations in testicular venous plasma.


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.


1997 ◽  
Vol 152 (1) ◽  
pp. 147-154 ◽  
Author(s):  
A Tohei ◽  
M Akai ◽  
T Tomabechi ◽  
M Mamada ◽  
K Taya

Abstract The functional relationship between thyroid, adrenal and gonadal hormones was investigated using adult male rats. Hypothyroidism was produced by the administration of 4-methyl-2-thiouracil (thiouracil) in the drinking water for 2 weeks. Plasma concentrations of TSH dramatically increased, whereas plasma concentrations of tri-iodothyronine and thyroxine decreased in thiouracil-treated rats as compared with euthyroid rats. Hypothyroidism increased basal levels of plasma ACTH and pituitary content of ACTH. The pituitary responsiveness to CRH for ACTH release markedly increased, whereas the adrenal responsiveness to ACTH for corticosterone release decreased. These results indicated that hypothyroidism causes adrenal dysfunction in adult male rats. Pituitary contents of LH and prolactin decreased in hypothyroid rats as compared with euthyroid rats. In addition, hypothyroidism lowered pituitary LH responsiveness to LHRH. Testicular responsiveness to human chorionic gonadotrophin for testosterone release, however, was not different between euthyroid and hypothyroid animals. These results indicated that hypothyroidism causes adrenal dysfunction and results in hypersecretion of ACTH from the pituitary gland. Adrenal dysfunction may contribute to the inhibition of LHRH secretion from the hypothalamus, possibly mediated by excess CRH. Journal of Endocrinology (1997) 152, 147–154


1991 ◽  
Vol 6 (1-2) ◽  
pp. 185-191 ◽  
Author(s):  
P.S.P. Gupta ◽  
P.C. Sanwal ◽  
V.P. Varshney

Endocrinology ◽  
1973 ◽  
Vol 92 (4) ◽  
pp. 1223-1228 ◽  
Author(s):  
A. BARTKE ◽  
R.E. STEELE ◽  
N. MUSTO ◽  
B.V. CALDWELL

1985 ◽  
Vol 38 (4) ◽  
pp. 445 ◽  
Author(s):  
Y M Hodgson ◽  
DM de Kretser

The testosterone responses to a single injection of HCG (100 i.u.) in hypophysectomized (hypox.), cryptorchid or sham-operated rats were followed over a 5-day period. In sham-operated rats, hCG induced a biphasic rise in serum testosterone, peaks being observed at 2 and 72 h. Reduced testis weights, elevated FSH and LH levels and reduced serum testosterone levels were found after 4 weeks of cryptorchidism, but hCG stimulation resulted in a normal 2 h peak in serum testosterone. However, the secondary rise at 72 h in cryptorchid rats was significantly lower than sham-operated rats.


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