Search Results

You are looking at 1 - 3 of 3 items for

  • Author: C. L. Au x
  • All content x
Clear All Modify Search
Free access

C. L. Au, D. M. Robertson, and D. M. de Kretser

Summary. The testicular inhibin content showed an initial increase in the first 2–3 days after bilateral ligation of the efferent ducts of rats, followed by a subsequent decline to levels significantly below normal by 14 days, and reached 25% of control values at 42 days. Serum concentrations of FSH and LH were significantly increased at Day 6–7 after treatment and were still elevated after 42 days. The decline in testicular inhibin content at times associated with elevated FSH concentrations is consistent with the hypothesis of inhibin being involved in the feedback control of FSH secretion.

Free access

C. L. Au, D. M. Robertson, and D. M. de Kretser

Summary. The concentrations of inhibin in samples of rat testicular venous and arterial blood and interstitial fluid were measured by an in-vitro bioassay using pituitary cells in culture in which the standard was an ovine testicular lymph preparation (assigned potency 1 unit/mg). Inhibin levels were undetectable ( < 2 U/ml) in both blood samples but reached a mean concentration of 120 ± 7 U/ml in testicular interstitial fluid. After unilateral efferent duct ligation the rate of inhibin accumulation in seminiferous tubules was determined by the difference in the inhibin content of the ligated and unligated testes. Additionally, the rate of seminiferous tubule fluid production was obtained from the difference in weight between the ligated and non-ligated testes. In the 24 h after efferent duct ligation there were linear increases in inhibin (18·5 ± 1·0 U/h) and in seminiferous tubule fluid production (26 ± 1 μl/h), but there were no changes in serum FSH and LH levels.

Experimental induction of bilateral cryptorchidism led to a decrease in the inhibin content of the testis after 10 days. The rate of inhibin accumulation after efferent duct ligation declined more rapidly than the inhibin content, being significantly depressed in cryptorchid testes after 3 days, suggesting that this measurement is a more sensitive index of inhibin production than the determination of testicular inhibin content.

Free access

C. L. Au, D. C. Irby, D. M. Robertson, and D. M. de Kretser

Summary. Rats were given s.c. implants of high (HT) or low (LT) doses of testosterone and 10 days later hypophysectomy or sham-operation was performed. The rats were killed after 50 days. Unilateral efferent duct ligation was performed 16 h before death to measure seminiferous tubule fluid production and the increment in testicular inhibin values (inhibin production). Inhibin levels in testis cytosols were measured by a pituitary cell culture bioassay. The LT implants maintained serum testosterone at control values and decreased testicular weight whereas HT implants raised serum testosterone 3-fold and maintained testicular weight at 75–85% of pretreatment levels. In intact rats, LT implants caused no change in testicular inhibin content but decreased inhibin production; no significant changes occurred with HT implants. After hypophysectomy both values were significantly suppressed and could not be maintained by HT or LT implants. However, the HT implants partly restored inhibin production despite their inability to influence testicular inhibin content. In contrast, tubule fluid production depended mainly on intratesticular testosterone levels and occurred normally in intact or hypophysectomized rats with HT but not LT implants. These results indicate that inhibin and seminiferous tubule fluid production, both functions of the Sertoli cell, are under different hormonal control. The maintenance of inhibin production by the testis requires the support of pituitary hormones, presumably FSH, while seminiferous tubule fluid production requires testosterone, presumably through LH stimulation of Leydig cells. These findings are consistent with the hypothesis that inhibin is produced in response to trophic stimulation by FSH.