Defect in the Renal Tubular Reabsorption of Water Associated With Potassium Depletion in Rats’ WALTER HOLLANDER, JR.,2 ROBERT W. WINTERS,” T, FRANKLIN WILLIAMS: JOHN BRADLEY, JEAN OLIVER AND LOUIS G. WELT

HOLLANDER, WALTER, JR., ROBERT W. WINTERS, T, FRANKLIN WILLIAMS, JOHN BRADLEY, JEAN OLIVER AND LOUIS G. WELT. Defect in the renal tubular reabsurption of water associated with potassium depletiun in rats. Am. J. Physiol. I&J(~): 557-563. q57.---The effect of graded degrees of K depletion on the ability to produce a concentrated urine was studied in Sprague-Dawley rats. With increasing degrees of K depletion, as measured by the concentration of K in fat-free skeletal muscle, there was a progrossive decrease in the maximum urinary concentration. This defect of the renal concentrating mechanism appeared to be better correlated with the degree than with the duration of potassium depletion and could be demonstrated either by the use of exogenous vasopressin or by water deprivation. The potassium-deficient rats in at least one experiment developed a significant polydipsia. The data do not allow any conclusions with respect to the relationship of the polydipsia to the renal concentrating defect except that the latter at least was not severe at the onset of the increased water intake. I N 1937, Schrader, Prickett and Salmon (I) reported lesions in the renal tubular epithelium of rats fed a diet deficient in potassium. This observation has been amply confirmed, although there has been no agreement as to the nature or location of the histologic abnormalities (2-4). In recent years much evidence has been obtained which suggests that depletion of potassium may result in derangements of renal function. A defect in the renal concentrating mechanism has been specifically suggested by the studies of Smith and Lasater (s), of Brokaw (6), of Spargo (4) and particularly by the recent studies in man of Relman and Schwartz (7). The present experiments represent an atReceived for publication December 28, 1956. l Aided by Research Grant H-1301(C3), from the National Institutes of Health. 2 Done during tenure of a postdoctoral research fellowship of the Public Health Service. 3 Done in part during tenure of a postdoctoral research fellowship of the National Foundation for Infantile Paralysis. 4 Done during tenure of a postdoctoral research fellowship of the Life Insurance IMedical Research Fund. tempt to study the effects of graded degrees of potassium depletion on the renal concentrating mechanism of the rat. A separate report (J.O.) will deal with the associated renal pathology. METHODS AND MATERIALS Experiment A. The animals were male, SpragueDawley rats with initial weights of 3oo-400 gm, housed in individual cages. All rats had free access to distilled water and to a basal diet which was deficient in potassium, sodium, phosphate and chloride, and which contained 4% urea, The composition of the diet is shown in table I, All rats were given 5 ml of an electrolyte solution once each day by gavage, control groups receiving normal amounts of potassium chloride and of a neutral mixture of monosodium and disodium phosphates, potassium-deficient groups receiving sodium bicarbonate and the same mixture of sodium phosphates. The quantities of each ion received in this manner are shown in table 2. The total solute load administered by gavage was the same for control and for experimental rats. After I and 2 weeks on the experimental regimen (groups AI and A-z), the ability of each rat to form a maximally concentrated urine was tested with exogenous vasopressin as described below. Approximately 24 hours after completing the renal concentration test, during which time the rats were again allowed free 557 by 10.0.33.2 on July 1, 2017 http://ajple.physiology.org/ D ow nladed fom d3 WALTER HOLLANDER, JR. ET AL. TABLE I. CONSTITUENTS OF THE BASAL DIET