THE EFFECT OF VARIOUS PHARMACOLOGICAL AGENTS ON THE MORPHOGENETIC ACTIONS OF ESTRADIOL

¹ From the Department of Anatomy, McGill University, Montreal, Canada

The effect of various pharmacological agents (mainly steroids) on the morphological changes induced by estradiol has been studied in the rat. The findings which are given in a table are not suitable for brief presentation in the form of a summary but the following salient facts may be mentioned:

Among all compounds examined androstenediol proved most potent in preventing the body weight loss caused by estradiol. It also proved to have the greatest preputial gland stimulating effect although its testoid action—judged by the ability of the compound to enlarge the seminal vesicles, prostates and coagulating glands—is much inferior to that of other steroids in our series (methyl testosterone, testosterone).

Few steroids are able to prevent the pituitary and adrenal hypertrophy elicited by estradiol overdosage. The most clear-cut inhibition of the hypophyseal hypertrophy was obtained with high doses of testosterone and methyl testosterone. The adrenal weight increase was not only prevented, but actually reversed by desoxycorticosterone acetate.

The thymus involution caused by estradiol is accentuated by most hormonally active steroids.

Definite proof is furnished that the ability of steroids to protect the testis against the atrophy caused by estradiol is entirely independent of their "male hormone" or testoid activity. Ethinyl testosterone, though a potent testoid, is not gonad-protecting while the reverse is true of pregnenolone.

The decrease in kidney weight caused by estradiol is effectively prevented only by highly active testoids such as testosterone and methyl testosterone.

On the basis of examples furnished by the present experimental series it is emphasized that by the use of suitable steroid hormone combinations it is possible to accentuate certain desired effects and simultaneously inhibit some of the undesirable side effects of hormones thus increasing the pharmacological specificity of their action.