Broulik P, Stárka L, Ston J
Physiol Bohemoslov. 1975;24(3):221-7.
The loss of endogenous testosterone in castrated male mice leads to a marked decrease in seminal vesicle and kidney tissue weight. 21 days' administration of exogenous testosterone abolished the effect of castration on the seminal vesicles and kidney tissue. The antiandrogen cyproterone acetate produced significant changes in the target tissue for androgens, i.e. in the seminal vesicles. In every case it blocked the action of both exogenous and endogenous testosterone on the seminal vesicles, but failed to block the "renotropic" action of testosterone, expressed as relative kidney weight. Contrary to its effect on the seminal vesicles, it did not influence relative kidney weight in normal animals. It likewise did not block the effect of exogenous testosterone on kidney tissue. The mechanism of the action of cyproterone acetate in androgen-dependent tissues is known to consist in inhibition of androgen binding to specific cell receptors in the target tissues. Some of the specific androgen receptors in mouse kidney are evidently different in character from those in the accessary sex glands, that being the reason why cyproterone acetate has an antiandrogenic, but not an antirenotropic effect. In agreement with experiments on rats, adrenal weight also decreases in mice after the administration of cyproterone acetate.
去势雄性小鼠内源性睾酮的丧失导致精囊和肾脏组织重量显著下降。给予外源性睾酮21天消除了去势对精囊和肾脏组织的影响。抗雄激素醋酸环丙孕酮在雄激素的靶组织即精囊中产生了显著变化。在每种情况下,它都阻断了外源性和内源性睾酮对精囊的作用,但未能阻断以相对肾脏重量表示的睾酮的“促肾生长”作用。与其对精囊的作用相反,它对正常动物的相对肾脏重量没有影响。它同样也没有阻断外源性睾酮对肾脏组织的作用。已知醋酸环丙孕酮在雄激素依赖性组织中的作用机制在于抑制雄激素与靶组织中特定细胞受体的结合。小鼠肾脏中的一些特定雄激素受体在性质上显然与附属性腺中的不同,这就是醋酸环丙孕酮具有抗雄激素作用但不具有抗促肾生长作用的原因。与对大鼠的实验一致,给予醋酸环丙孕酮后小鼠的肾上腺重量也会下降。