THE EFFECT OF SALT DEPRIVATION ON THE URINARY CONCENTRATING MECHANISM IN THE DOG*

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Abstract
Urinary concentrating ability was studied in dogs before and after sodium restriction by measuring maximum urinary concentration and TCH2O (tubular clearance of H2O) formation during mannitol diuresis. Sodium deprivation resulted in a slight fall in maximum osmotic urine/plasma ratios and a marked fall in TCH2O formation so that hyptotonic urine was excreted at moderate urine flows, This alteration in urinary concentrating ability was not due to an increased aldosterone secretion, since exogenous aldosterone failed to produce it in sodium- fed dogs and aldosterone antagonists failed to correct it in sodium-deprived dogs. The defect, however, was always associated with a fall in glomerular filtration rate (GFR) and was corrected by raising GFR in salt-restricted dogs with methylprednisolone. That diminished GFR did not produce the defect by decreasing the amount of sodium reaching the loop of Henle was shown by the ability of sodium-fed hyponatremic dogs to form normal TcH2O despite a reduction in sodium delivery to the loop of Henle to levels far below those of normonatremic sodium-deprived dogs. It is concluded that the defect in urinary concentration seen in sodium deprivation is due to the failure of distal tubular fluid to equilibrate to isotonicity before reaching the collecting tubule.