We studied the role of catecholamines in the regulation of potassium homeostasis in nine healthy subjects given intravenous potassium chloride (0.5 meq per kilogram of body weight) in the presence and absence of propranolol. Potassium infusion elevated serum potassium 0.6±0.09 meq per liter (mean ±S.E.M.). Addition of propranolol augmented the rise (0.9±0.05 meq per liter) and prolonged the elevation in serum potassium without decreasing urinary potassium excretion. In a separate study, the same potassium load was administered with a concomitant infusion of epinephrine in five subjects. Epinephrine markedly blunted the increment in serum potassium (0.1±0.06 meq per liter) while reducing renal potassium excretion. Plasma aldosterone was not altered by the experimental procedures. Serum insulin fell minimally in the presence of propranolol but was unaffected by epinephrine. β-Adrenergic blockade impairs and epinephrine enhances extrarenal disposal of an acute potassium load. These findings suggest that in patients with impaired potassium disposal, the risk of hyperkalemia may be increased when sympathetic blockade is induced. (N Engl J Med. 1980; 302:431–434.) A ROLE of catecholamines in the regulation of plasma potassium concentration was suggested when D'Silva observed a marked decline in potassium concentration after injection of epinephrine in cats.1 , 2 Subsequent studies revealed this effect to be greater with epinephrine than norepinephrine,3 and experiments in pancreatectomized4 or insulindeficient and nephrectomized animals5 , 6 have demonstrated that the hypokalemic effect of epinephrine is independent of insulin, aldosterone, and renal excretion of potassium. Recent clinical reports have also suggested that β-adrenergic blockade impairs potassium tolerance in man.7 , 8 This investigation was undertaken to explore more fully the effect of catecholamines on the acute disposition of a small. . .
ASJC Scopus subject areas