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1. Testosterone propionate (0.5 mg/day) administered for 5 weeks to prepubertal rats increased the weight of sex accessory organs but did not alter the rate of gain of body weight. Methandienone, given in a similar dosage regimen, was without effect on these parameters. The synthetic progestagen, norgestrel, administered orally in a dose of 0.5 mg/day increased the weight of the vas deferens but was without effect on seminal vesicle and testis weights and on the growth rate. Given in combination with testosterone, norgestrel caused a marked decrease in testis weight and reversed the effects of testosterone propionate on seminal vesicle weight. Thus, in the dosage regimen used, this progestagen exhibited an endocrine profile comprising androgenic, synandrogenic and anti-androgenic effects.2. Rats, which were castrated when they weighed 70-80 g, exhibited rates of gain of body weight which were similar to those of control animals. Testosterone propionate in the doses used reversed castration-induced atrophy of the vas deferens and seminal vesicle.3. The contractility of the vas deferens of intact rats, determined by direct field electrical stimulation, was unaffected by treatment with the steroids used in this study. However, there was a marked impairment of the contractility of the vas deferens following castration, which was not fully restored by testosterone propionate in the dosage regimen used.4. The efficacies and potencies of the a-adrenoceptor agonists phenylephrine and I-metaraminol in causing contraction of the vasa deferentia from intact rats were unaffected by the steroid treatments. In contrast, these agonists did not produce sustained, dose-dependent contractions of the vasa deferentia from castrated rats; however testosterone propionate fully restored the efficacy and potency of both agonists. 5. It is concluded from this study that although adequate testosterone levels are necessary for the maintenance of contractility in the rat vas deferens, the integrity of postjunctional adrenoceptors is not modified by a variety of steroid treatments.
1. Testosterone propionate (0.5 mg/day) administered for 5 weeks to prepubertal rats increased the weight of sex accessory organs but did not alter the rate of gain of body weight. Methandienone, given in a similar dosage regimen, was without effect on these parameters. The synthetic progestagen, norgestrel, administered orally in a dose of 0.5 mg/day increased the weight of the vas deferens but was without effect on seminal vesicle and testis weights and on the growth rate. Given in combination with testosterone, norgestrel caused a marked decrease in testis weight and reversed the effects of testosterone propionate on seminal vesicle weight. Thus, in the dosage regimen used, this progestagen exhibited an endocrine profile comprising androgenic, synandrogenic and anti-androgenic effects.2. Rats, which were castrated when they weighed 70-80 g, exhibited rates of gain of body weight which were similar to those of control animals. Testosterone propionate in the doses used reversed castration-induced atrophy of the vas deferens and seminal vesicle.3. The contractility of the vas deferens of intact rats, determined by direct field electrical stimulation, was unaffected by treatment with the steroids used in this study. However, there was a marked impairment of the contractility of the vas deferens following castration, which was not fully restored by testosterone propionate in the dosage regimen used.4. The efficacies and potencies of the a-adrenoceptor agonists phenylephrine and I-metaraminol in causing contraction of the vasa deferentia from intact rats were unaffected by the steroid treatments. In contrast, these agonists did not produce sustained, dose-dependent contractions of the vasa deferentia from castrated rats; however testosterone propionate fully restored the efficacy and potency of both agonists. 5. It is concluded from this study that although adequate testosterone levels are necessary for the maintenance of contractility in the rat vas deferens, the integrity of postjunctional adrenoceptors is not modified by a variety of steroid treatments.
Testosterone administration to female mice for 25 days produced a 70% increase in total kidney protein in both A/J and C57BL/6J mice. This is in contrast to the known androgen-responsive proteins, such as beta-glucuronidase and alcohol dehydrogenase, which each represent less than 1% of the total kidney proteins even after maximum stimulation. To investigate this discrepancy, we initiated a study to identify major proteins which increase with androgen treatment. Three new cytoplasmic proteins designated T1, T2, and T3 were found in different subcellular fractions of both A/J and C57BL/6J mice. T1 (43,000 daltons) and T2 (60,000 daltons) were found in the mitochondrial-lysosomal fraction of 25-day androgen-treated mice. T3 (54,000 daltons) was found in the microsomal fraction. Each of these proteins increased several-fold during androgen treatment, so that they were easily identified using sodium dodecyl sulfate polyacrylamide gel electrophoresis. By contrast, no major changes were noted in the soluble proteins. A nonhistone chromosomal protein of 54,000 mol wt (T4) was found in chromatin preparations from androgen-stimulated A/J mice. Additional studies with androgen-insensitive Tfm/Y mice and with various hormones indicated that stimulation of the T proteins was dependent on androgenic steroid and a functional androgen receptor.
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