Adrenal Hormones and the Regulation of Serum Potassium in Potassium-Loaded Adrenalectomized Dogs*

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Abstract
In dogs, tolerance to infusion of 2 meq KCl/kg/h stems largely from an ability to transfer about % of the administered K from extra- to intracellular fluid. Also involved are the quantity of K lost in the urine and the heart's intrinsic sensitivity to K, i.e. its ability to withstand increased concentrations of serum K without developing electrocardiogram changes of advanced hyperkalemic cardiotoxicity. Bilateral adrenalectomy produces a highly significant reduction of tolerance to KC1 infusion. The reduction arises partly from a highly significant decrease in the proportion of infused K transferred to intracellular fluid (this is accompanied by a striking fall of the serum insulin response to KC1 infusion), partly from a marked increase of cardiac sensitivity to K, and, to some extent, from a decrease in urinary K loss. Treatment with adrenal hormones (aldosterone, dexamethasone, hydrocortisone, or epinephrine) affects one or more of the factors involved in tolerance to KC1 infusion. Treatment with each of the adrenal hormones decreases cardiac sensitivity to K, but treatment with glucocorticoids is the most effective. The porportion of infused K lost in the urine is increased only by treatment with steroid hormones; in hyperkalemic adrenalectomized dogs, glucocorticoids are far more powerful kaluretics than aldosterone. Epinephrine is the only adrenal hormone involved in K transfer. Treatment with epinephrine increases the proportion of infused K transferred to intracellular fluid to the level found in K-loaded intact control dogs; the increased K transfer ability is unaccompanied by a significant rise of serum insulin.