450 ANNUAL REPORT SMITHSONIAN INSTITUTION, 1957 



chloride values in patients with adrenal insufficiency are associated 

 with continued urinary losses and are accompanied by low potassium 

 excretion and increased serum potassium values. These changes are 

 prevented by the normal secretion of the adrenal cortex involving 

 steroids such as deoxycorticosterone, cortisone, and aldosterone. 

 However, these hormones not merely influence sodium chloride and 

 potassium salt metabolism but also play an important part in the 

 regulation of protein metabolism (increased urea excretion in hyper- 

 adrenalism), carbohydrate metabolism (diabetes in adrenal hyper- 

 function; hypoglycemia in adrenal insufficiency), blood pressure 

 (hypertension in adrenal hyperfunction ; low blood pressure in 

 adrenal insufficiency), fat metabolism (changes in fat distribution in 

 adrenal hyperfunction), pigment metabolism (discoloration in ad- 

 renal insufficiency). If, then, certain body functions are directly 

 influenced by the adrenal cortical hormones, one might ask whether 

 the intake of sodium chloride affects them because of its intimate 

 relationship with adrenal function. 



Abundant proof has been given that the deleterious effects of ad- 

 renal insufficiency can be at least partially counteracted by the ad- 

 ministration of salt. This is true both for humans suffering from 

 Addison's disease and adrenalectomized animals. On the other hand, 

 salt intake is clinically undesirable in conditions in which the induc- 

 tion of hyperadrenalism is a disadvantage. As is known, the ad- 

 ministration of either cortical hormones or salt may lead to similar 

 symptoms in circulatory conditions, hypertension, and the like. 



There exists by now a considerable body of evidence linking the 

 functions of the cortical hormones to those of salt. Thus, hypertension 

 produced by deoxycorticosterone is enhanced by simultaneous admin- 

 istration of sodium chloride. The kidney lesions and changes in food 

 and water intake brought on by salt are potentiated by cortisone. 

 There exists, furthermore, a considerable similarity in the influence 

 which the adrenal cortex or salt exerts on carbohydrate metabolism. 

 Hyperadrenalism is accompanied by increased deposition of glycogen 

 in the liver and a high blood sugar. On account of the simultaneously 

 increased urea excretion, it was deduced that the increased glycogen 

 formation is due to catabolic processes in protein metabolism. The 

 administration of salt leads to similar changes, namely, increased 

 deposition of glycogen, reduced oxidation of glucose leading to in- 

 creased blood sugar, and increased urea excretion. On the other hand, 

 the reduced intestinal absorption of glucose on adrenalectomized 

 animals can be equally corrected by a salt or by adrenal hormones. 

 Unless one assumes that this latter finding is only due to improved 

 intestinal blood supply, a more specific salt effect becomes probable, 

 which leads to the conclusion that the effects of salt and of adrenal 



