Measurement of sodium-retaining substances in human urine.

Recognition of the role of the adrenal cortex in electrolyte metabolism dates back to 1927 (1,2). Since then, a great deal has been learned about the effects ot adrenalectomy, and replacement therapy, on electrolyte metabolism. A number of adrenal cortical compounds have been isolated, and their biological activity in adrenalectomized animals, and in patients with Addison’s disease, has been ascertained. No attempt will be made, in this section, to cover all of the findings reported on the subject of the adrenal cortex and electrolytes, as several excellent reviews have appeared in recent years (3,4,5). However, some findings, pertinent to the present study, are presented below. In 1932, Loeb (6) found that there was a fall in plasma sodium in Addisonian crisis, and that the administration of sodium chloride would render the patient symptom-free (7). The fall in plasma sodium following adrenalectomy in the dog was related to the abnormally large quantity of sodium in the urine (8). This urinary loss of sodium was attributed, by Harrison and Darrow (9), to a disturbance in the tubular reabsorption of this ion from the glomerular filtrate. Anderson and co-warkers noted that adrenalectomized rats, unsupported by salt treatment, had increased total sodium excretion, and an increased rate of excretion of administered sodium-24, as compared with normal animals (10,11,12). They found the reverse to be true for potassium.[...