ANTIDIURETIC HORMONE CONTENT OF THE HYPOTHALAMO-NEUROHYPOPHYSIAL SYSTEM AND URINARY EXCRETION OF ANTIDIURETIC HORMONE IN RATS DURING THE DEVELOPMENT OF DIABETES INSIPIDUS AFTER LESIONS IN THE PITUITARY STALK

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Abstract
SUMMARY: The antidiuretic hormone (ADH) content of the hypothalamo-neurohypophysial system (HNS) and the excretion of AD-activity in the urine has been examined after pituitary stalk lesion in rats. In the oliguric phase which developed approximately 24 hr. after stalk destruction and lasted for about 3 days, the HNS was greatly depleted of ADH and the excretion of AD-activity in the urine was much above normal. Implantation of posterior lobes obtained from intact adult rats under the kidney capsule of stalk-lesioned animals with a manifest diabetes insipidus produced oliguria similar to that found after stalk destruction. However, the antidiuretic effect of the implant lasted somewhat longer and the amount of AD-activity excreted in the urine was twice as high as that excreted in the oliguric period after stalk destruction. Subcutaneous injection of lysine or arginine vasopressin in various vehicles into rats with manifest diabetes insipidus showed that the effect of these preparations on water intake and urine output was independent of the dosage used but seemed to depend on the rate of absorption from the subcutaneous tissue. The results indicate a relationship between duration of action and the amount of AD-activity excreted in the urine. Hyperosmoticity induced by the subcutaneous injection of a 15% NaCl solution failed to release ADH irrespective of the hormone content of the HNS of stalk-lesioned rats. In a number of stalk-lesioned rats the polyuria gradually disappeared several weeks after stalk destruction. The ADH content of the hypothalamus of these animals was nearly normal, but that of the posterior lobe was only about 10 % of that of intact controls. The urinary excretion of AD-activity in these animals was about half of that of the controls. In such rats ADH could be readily released from the HNS after loading with 15% NaCl, indicating that animals with a regression of the diabetes insipidus had resumed the production of ADH.