Adrenergic Modulation of Extrarenal Potassium Disposal

TLDR

They administered intravenous potassium chloride to healthy subjects with and without propranolol, and separately with epinephrine, to assess catecholamine effects on potassium homeostasis. Potassium infusion raised serum potassium by 0.6 mEq/L, an effect amplified to 0.9 mEq/L and prolonged by propranolol without reducing urinary excretion, while epinephrine blunted the rise to 0.1 mEq/L and decreased renal excretion, and aldosterone and insulin were largely unchanged, showing that β‑adrenergic blockade impairs and epinephrine enhances extrarenal potassium disposal, increasing hyperkalemia risk when sympathetic blockade is induced. N Engl J Med 1980; 302:431–434.

Abstract

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.)