Phosphate infusions were given to human subjects at a rate which elevated the plasma concentration to three or four times the normal level, and then permitted to fall slowly. In subjects who had taken cortisone by mouth, the plasma phosphate concentration was lower before and throughout the infusion.
Phosphate infusions were also given at a rate which for many hours maintained the plasma concentration at about double the normal level. Intravenous injection of hydrocortisone caused, after a latent period of about 1¼ hr, a sharp fall in plasma phosphate.
Hydrocortisone given intravenously without previous phosphate infusion led, after a similar latency, to a sharp fall in plasma phosphate. Since the phosphate did not appear in the urine, and the volume of extracellular fluid did not expand under the influence of glucocorticoids, it is inferred that the phosphate had become intracellular.
Intravenous hydrocortisone had little effect upon plasma potassium. It produced a small and variable rise in plasma glucose, a small rise in oxygen consumption without consistent change in r.q., and no change in plasma pH.
Oral glucose followed by intravenous insulin caused a large drop in plasma potassium and a small one in plasma phosphate.
Intravenous deoxycorticosterone, in doses which caused a similar sodium retention to that produced by hydrocortisone, did not depress plasma phosphate concentration.
The possible relationship between the changes in plasma electrolytes and carbohydrate metabolism is discussed.