The sexually differentiated activity of rat kidney cytoplasmic 17.beta.-hydroxysteroid dehydrogenase is subject to multihormonal regulation. Gonadectomy and the treatment of intact male animals with estradiol removes the repressive influence of testicular androgens, thereby allowing the male animal to reach the higher female level. The maintenance of this sexually undifferentiated activity level is a function of the thyroid gland, the adrenals and of growth hormone (somatotropin) and prolactin. Removal of the thyroid or the adrenals from intact animals decreases the activity and eliminates the sexual difference. Following the substitution of hypophysectomized animals with different hypophyseal hormones or gonadotropin preparations, only growth hormone and prolactin are effective in causing an increase in the very low activity. The sexual differentiation of renal 17.beta.-hydroxysteroid dehydrogenase activity observed in intact rats is clearly the result of the repressive action of testicular androgens on a multihormonally controlled activity level.