Abstract
Conclusions
Commercial and synthetic vasopressin are equipotent in producing ascorbic acid depletion in rats with those hypothalamic lesions which prevent the adrenal response to certain non-specific stimuli. The results are interpreted to mean that vasopressin can evoke ACTH release in these animals and that the ACTH-releasing activity of neurohypophyseal extracts, when tested in vivo, is accounted for by their content of vasopressin. The results support the hypothesis that vasopressin (ADH) is the neurohumor responsible for ACTH release.
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