Abstract
Triiodothyronine or thyroxine administration (100 [mu]g daily, 7[long dash]14 days) to rats with chronic median eminence lesions (26[long dash]210 days) increased adrenal weight without correcting pituitary and ovarian atrophy, decreased adrenal and ovarian ascorbic acid concentrations, and elevated plasma and adrenal corticoid levels. Depletion of ascorbic acid in endocrine glands also occurred in hypo-physectomii-ed rats chronically treated with T,: no significant effect was found on adrenal weight or corticosteroid content. Dinitrophenol produced no substantial change in any indices of adrenal cortical function. Electrical stimulation of the anterior hypothalamus in intact rats stimulated ACTH release. The effect was completely blocked in rats bearing median eminence lesions. The results signify that basal ACTH secretion following long-term destruction of the median eminence is appreciable and can be enhanced by severe hyperthyroidism; ascorbic acid depletion in target endocrines is not a reliable index of pituitary trophic hormone activity in hyperthyroidism; neural stimuli from the rostral hypothalamus mediate their effects on ACTH release via the median eminence; and augmentation of ACTH secretion in severe hyperthyroidism involves a non-neural, humoral metabolic pathway.