scholarly journals Testosterone Response of Cryptorchid and Hypophysectomized Rats to Human Chorionic Gonadotrophin (hCG) Stimulation

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.

1989 ◽  
Vol 121 (2) ◽  
pp. 311-316 ◽  
Author(s):  
S. Maddocks ◽  
B. P. Setchell

ABSTRACT We have used a push–pull cannula to collect interstitial fluid from the testes of anaesthetized rats at various times after a single injection of human chorionic gonadotrophin (hCG; 50 IU), and compared the levels of testosterone in this fluid with the levels in testicular and peripheral venous blood collected at the same times. Following hCG injection, significant increases in testosterone concentrations were observed in all fluids with notable peaks occurring in interstitial fluid at 2, 8 and 24 h, in testicular venous blood at 2, 8 and 30 h, and in peripheral venous blood at 2, 8, 24 and 72 h. The results demonstrate for the first time that changes in testosterone concentrations in interstitial fluid can be different from those in testicular venous blood. In addition, when testosterone levels in interstitial fluid were compared with levels in testicular venous blood at each time-point, the results suggested that the partitioning of testosterone between these two compartments can be regulated. Furthermore, the changes in both interstitial fluid and testicular venous blood levels of testosterone do not always parallel those in peripheral venous blood, suggesting that changes in testicular blood flow and peripheral clearance rates of testosterone may also be important in the control of circulating testosterone concentrations. Journal of Endocrinology (1989) 121, 311–316


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.


1965 ◽  
Vol 33 (3) ◽  
pp. 447-454
Author(s):  
M. J. K. HARPER

SUMMARY Administration of chlormadinone, an orally active progestational agent without significant oestrogenic activity, to intact immature female rats did not affect either ovarian or uterine weight significantly compared with controls. A single injection of human chorionic gonadotrophin (HCG) caused a 73 % increase in uterine weight in 24 hr. over the control value. This dose significantly increased ovarian weight and although it caused some stimulation of follicular development, ovulation during this time did not occur. When animals were treated with chlormadinone for 8 days, and received HCG on the 8th day, uterine weight was 170% greater than in the controls and 56% greater than with HCG alone. The uterine weight produced was similar to that found in animals treated with mestranol, a potent oestrogen, and HCG. In ovariectomized animals HCG did not affect uterine weight, while the small increase produced by chlormadinone was unaltered when HCG also was given. Mechanisms are discussed by which this augmentation of the uterine response to HCG might be produced. It seems most likely that chlormadinone administration causes storage of endogenous gonadotrophin in the pituitary, and that the exogenous gonadotrophin acts as the 'trigger' for the release of stored hormone, probably by a direct action on the hypothalamus.


Author(s):  
N. Walker ◽  
P. J. Burnett

Puberty can be stimulated from about 160 days of age by the introduction of a mature boar usually in accomodation which is novel to the gilt. The interval between stimulation and response is not always predictable and therefore does not facilitate the synchronisation of gilt matings with the mating pattern in an established sow herd. It has been reported previously that a single injection of pregnant mares’ serum gonadotrophin (PMSG) pits human chorionic gonadotrophin (HCG)* will initiate puberty. The investigations reported here concern the use of these exogenous hormones as an additional or alternative stimulus to those described above.


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


1964 ◽  
Vol 45 (4_Suppl) ◽  
pp. S179-S190 ◽  
Author(s):  
G. A. Overbeek ◽  
J. de Visser

ABSTRACT Lynestrenol and 6α-methyllynestrenol were studied in rats for their respective ability to: prevent spontaneous ovulation. prevent ovulation induced by a single injection of luteinizing hormone (human chorionic gonadotrophin). to prevent ovarian hypertrophy in parabiotic (♀[unk]) rats The results warrant the following conclusions about the site of action of both substances: Lynestrenol prevents ovulation by inhibiting FSH release from the pituitary gland, so that there are no ripening follicles ready to respond to LH. 6α-Methyllynestrenol inhibits ovulation by abolishing LH-release thus preventing the final maturation and rupture of normally developing follicles.


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.


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