This Article  • References  • Full text PDF  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Social Bookmarking   What's this?

ALLEN D. KELLER, Ph.D.; J. WILLIAM HAMILTON, Jr., A.B.

Arch Surg. 1938;37(5):760-771.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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 . . . [Full Text PDF of this Article]

Author Affiliations
UNIVERSITY, ALA.

From the Department of Physiology and Pharmacology, the University of Alabama School of Medicine.

Footnotes
The work described in this paper was aided by a grant from the Rockefeller Foundation.

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?