Cause of Excessive Drinking in Diabetes Insipidus

Abstract

DAMAGE to the posterior lobe of the pituitary gland or in the region of the tuber cinereum of the hypothalamus causes diabetes insipidus, characterized by excessive drinking (polydipsia) and excessive production of urine (polyuria). Because both these effects are controlled by administration of posterior pituitary antidiuretic hormone which is known to act on the kidneys, it has been supposed that the polydipsia in diabetes insipidus is secondary to the polyuria caused by lack of antidiuretic hormone. Evidence for this view comes from experiments carried out by Richter and Eckert in 1935. They found that after removal of the posterior lobe of the pituitary gland in rats the resulting polydipsia is eliminated by tying both ureters to prevent urine formation¹. When urination is prevented in rats with diabetes insipidus caused by hypothalamic lesions, however, the results are not so straightforward. Electrolytic lesions made with a nichrome electrode at the base of the tuber cinereum, which invariably gave rise to diabetes insipidus in rats with their kidneys present, also slightly increased the water intake in rats with both kidneys removed². Such an excess drinking in diabetic rats without kidneys (primary polydipsia) would be important if, as Smith and McCann suggested, it could be shown to result from damage to a hypothalamic “thirst satiety centre” responsible for stopping drinking when sufficient water had been drunk to satisfy the body's needs.