SALT CONSUMPTION — KAUNITZ 449 



portant that a number of enzyme systems can only function if sodium 

 chloride is present at certain concentrations. In view of the fact 

 that we now believe that the life of the cell is maintained by enzymatic 

 processes, sodium chloride is an integral part of the cell. 



These dynamic equilibria are encountered in any living organism. 

 In higher animals they are, to a considerable extent, under hormonal 

 control, and disturbances of the more basic processes become notice- 

 able if the hormonal control breaks down. Thus, one finds that in 

 many diseases the sodium-potassium ratio in the tissues is disturbed, 

 which probably interferes with metabolic processes bound to a con- 

 stant sodium-potassium ratio. It is quite probable that in diseases 

 which are of generalized character and are also accompanied by signs 

 of renal damage, excess dietary salt can enhance the disturbances of 

 the sodium-potassium ratio in the tissues and can thus contribute to 

 the occurrence of metabolic failure; but these conditions are by no 

 means clear, and the influence of dietary salt in health and disease 

 can be better appreciated from its effect on the hormonal mechanisms 

 than from its action on the basic processes. 



The regulatory mechanisms of salt metabolism not only involve 

 incretory glands but also every major organ directly or indirectly. 

 One mechanism involving the central nervous system was discovered 

 by Claude Bernard, who demonstrated that injury to a certain part 

 of the medulla is followed by the excretion of large amounts of sodium 

 chloride. Although a great deal of thought has been given to the 

 central nervous regulation of mineral metabolism, neither its correla- 

 tion to other regulating mechanisms nor how it is affected by changes 

 in salt intake is clear. 



Renal mechanisms in salt metabolism have received considerable at- 

 tention. In fact, the salty taste of urine attracted the curiosity of 

 people for a long time, and this was the reason for its medicinal use. 

 Despite the enormous amount of work done since then on the ex- 

 cretory mechanism of the kidney, there is little evidence as to 

 whether the dietary intake of salt eventually interferes with the 

 excretory power. From an evolutionary point of view, it is well to 

 remember that sodium chloride is a scarce material for most animals 

 and is constantly reabsorbed by the kidney. Excess salt intake forces 

 the kidney to excrete rather than to reabsorb it, which may "prove 

 too much for it" in the long run. Such a view is supported by the 

 rapid occurrence of histological changes in the kidneys of animals 

 on a high dietary salt intake. 



The regulatory mechanism for sodium chloride metabolism at pres- 

 ent best understood rests in the adrenals. This function of the 

 adrenal cortex was educed in R. F. Loeb's studies on patients with 

 Addison's disease. It was demonstrated that the low serum sodium 



