Abstract

The existence of a physiological relationship between ACTH and gonads was recognized several years ago by Davidson & Moon (1936) who observed that the administration of this hormone to young castrated male rats caused a marked increase in the weight of the accessory reproductive organs. Davidson (1937) further reported that ACTH evoked similar responses in the accessory genitalia of male rats even after hypophysectomy but not after adrenalectomy. This indicated that ACTH probably stimulated the adrenal cortex to produce androgen. Nelson (1941) confirmed Davidson & Moon's findings and demonstrated that ACTH increased the weight of the seminal vesicles and the prostate of castrated rats. Subsequent studies, however, recorded somewhat erratic responses of the male genital organs after administration of this hormone (Li & Evans, 1947; Baker et al., 1950; Asling et al., 1951; Sprague, 1951: and Baker, 1952). Notwithstanding all such discrepancies, these findings were able to establish beyond

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