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Although aldosterone has recently been shown to play a part in the retention of sodium by edematous subjects (5), the factors governing its production have not been defined.It has been reported (6) that sodium restriction in normal subjects leads to increases in urinary aldosterone-like steroids, and that the quantities of such steroids are, other things being equal, inversely proportional to the amount of sodium excreted in the urine (5). In the studies reported here we have confirmed these reports in part, and have sought to clarify the mechanism or mechanisms by which changes in sodium balance lead to changes in aldosterone secretion. The evidence supports the view that some function of extracellular fluid volume, and not sodium per se, mediates the regulation of aldosterone secretion by dietary sodium. METHODSStudies were done on 18 normal control subjects, on one patient with diabetes insipidus and on one with panhypopituitarism. They were maintained on metabolic regimen, in air-conditioned environment; intake of food and fluids was changed only as the design of experiment required changes of salt and water intake. In four instances, only water, dextrose and sodium chloride were given throughout the study. Body weight was determined daily under standard conditions, and blood drawn at the start of metabolic days. Urine was collected in 24-hour lots. Serum and urine were analyzed for sodium and potassium by flame photometer, with lithium as internal standard, for chloride by the method of Van Slyke and Hiller (7) and for osmolality by the instrument designed by Bowman, Trantham, and Caulfield (8) using as standards sodium chloride solutions corrected for "true" osmolality with the use of the In-

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