The effect of salt deprivation

According to the countercurrent theory (1-3), concentration of the urine results from the movement of water from the collecting tubule into the hypertonic medullary interstitium. Medullary hypertonicity is generated and maintained by the sodium transported out of the ascending limb of the loop of Henle and trapped in the medulla by the vasa recta which form a countercurrent exchanger. Consequently, the availability of sodium for reabsorption in the loop of Henle may assume a critical role in the regulation of urinary concentration. Various derangements in water excretion have been detected when the intake or renal excretion of sodium is altered. Patients with congestive heart failure, cirrhosis of the liver, and other conditions characterized by diminished sodium excretion frequently have been reported to have impaired urinary concentration in the absence of intrinsic renal disease. Levinsky, Davidson and Berliner (4) noted that dogs maintained on a sodium-free diet showed decreased maximal urinary concentration. Levitt, Levy and Polimeros (5), however, found that salt restriction in normal human subjects for 5 days had no effect on maximal urinary concentration. The present studies were undertaken to examine the relationship of sodium metabolism to urinary concentrating ability by evaluating the effects of varying sodium intake, glomerular filtration rate (GFR), aldosterone activity, and serum