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Abstract
ABSTRACT The ACTH-releasing activity of synthetic oxytocin has been investigated in male rats, using adrenal ascorbic acid depletion as an indication of ACTH release. In acute experimental conditions synthetic oxytocin caused a highly significant adrenal ascorbic acid depletion in normal animals, as compared both to intact controls and to controls injected with physiological sodium chloride solution. It did not however, produce any adrenal ascorbic acid depletion in animals blocked by means of prednisolone. Administered as daily injections, synthetic oxytocin no longer caused any significant adrenal ascorbic acid depletion after six to nine days of treatment. It has been concluded that the ACTH-releasing activity of synthetic oxytocin is non-specific and thus is not the hypothalamic neurohumoral substance causing ACTH release from the anterior pituitary gland. The nature of this substance has been discussed in the light of previous results and of those obtained in the present investigations.
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