The theory that the secretory activity of the posterior lobe of the hypophysis is regulated in the mammal and in man through a diencephalic-hypophyseal mechanism has received wide recognition, although up to the present time little positive experimental evidence has been offered in support of this contention. In a recent series of articles evidence has been presented which indicates that the secretion of the antidiuretic principle by the posterior lobe is regulated through the supraoptic nuclei of the hypothalamus and the tracts which arise from them (1, 2, 3, 4). It has been shown that when the supraoptico-hypophyseal tracts are interrupted bilaterally in the cat and monkey by appropriate lesions in the anterior hypothalamus a diabetes insipidus develops which is always associated with marked degenerative changes in the pars nervosa and atrophy of the supraoptic nuclei. Because of the constant association of atrophy of the pars nervosa with diabetes insipidus in these forms, it was concluded that this disorder is due, in final analysis, to a diminution in or total abolition of the secretion of the antidiuretic principle by this division of the pituitary. This conclusion was further borne out by our finding and that of Richter (5) that the polyuria of diabetes insipidus is primary to the polydipsia.
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Fisher et al. (1936) studied this question.
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