The denervation theory of the causation of diabetes insipidus holds high interest at the present time. This theory is based on the assumption that diabetes insipidus is due to the absence of, or to a deficiency in, the antidiuretic principle which is elaborated by hypophysial tissue. It depicts that this tissue is activated only by neurogenic influences carried by the nerve fibers which take origin in the hypothalamus and pass to the hypophysis by way of the infundibular stalk.
In an early statement of the theory, the antidiuretic principle was assumed to be elaborated by the epithelial investment of the pars nervosa, namely, by both the pars intermedius and the pars tuberalis.1 Later, attention was focused on the infundibular process (the enlarged distal portion of the pars nervosa) as the secretory structure. This shift was largely due to the successful extraction of the antidiuretic principle from the neural lobes