Abstract

A relation of the adrenal cortex to potassium metabolism is substantiated by the following facts. In experimental adrenal insufficiency, and in Addison's disease there is a definite rise in plasma potassium. This high potassium can be lowered by injection of adrenal cortex extract. In adrenal insufficiency there is an increased susceptibility to exogenous potassium, which has been quantitatively contrasted with normal potassium tolerance in experimental animals. The application of potassium tolerance determinations in the human is here briefly described. Solutions of potassium salts were administered by mouth, the dose being 10 mg. or 20 mg. of K per pound of body weight. Duplicate determinations of potassium were done for plasma and whole blood taken from the finger or ear immediately before taking the drink, and at intervals of 30 min., 1 hr., and 2 hr., thereafter. Simultaneous hematocrit readings enabled us to calculate the red cell potassium content. If similar amounts of potassium contained in food are taken, slower assimilation makes it necessary to continue the test for 5 hours. Seventeen human potassium tolerance curves on 12 individuals have been completed to date. Since this preliminary paper does not permit detailed discussion of all the curves, a few typical ones only are shown. The plasma K of normal individuals is not affected by ingestion of 10 mg. K per pound body weight (Graph 1). In Addison's disease, however, there is a rapid and very considerable rise in plasma K (Graph 2), much greater than can be accounted for by hemoconcentration. At the end of 2 hours both cell volume and plasma K are again approaching the initial values, but the red cell K content has increased, the increase being perhaps compensatory.

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