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Luetscher & Johnson (1954) have recently shown that dietary restriction of salt in normal individuals results in an increase in the urine of a salt retaining compound which closely resembles aldosterone and which appears to be adrenocortical in origin. Until this discovery, only circumstantial evidence has supported the view that, with inadequate intake, the renal conservation of salt is accomplished by an increase in tubular reabsorption which is mediated by an adrenocortical hormone. This indirect evidence includes the histological studies of Deane, Shaw & Greep (1948) in rats and of Peschel & Race (1954) in human subjects besides observations upon the tubular reabsorption of salt by Black, Platt & Stanbury (1950) and upon the excretion of potassium by Leaf & Couter

OBSERVATIONS UPON THE WITHDRAWAL OF SODIUM CHLORIDE FROM THE DIET IN HYPERTENSIVE AND NORMOTENSIVE INDIVIDUALS