Abstract

Experiments were performed in anesthetized dogs to find the site of potassium uptake underlying the reduction of plasma [K] during the continuous infusion of epinephrine. In two groups of dogs, epinephrine (2 µg/kg/min) was infused i.v. Plasma [K] was measured 1) in a systemic artery and a femoral vein and 2) in a systemic artery and a hepatic vein. In both groups, arterial [K] increased, then fell below control by minute 10 of the infusion. In time first group, arterial [K] exceeded femoral venous [K] during time hyperkalemia and during the development of hypokalemia, indicating uptake of potassiunm by skeletal muscle. Propranolol reversed the hypokalemia. In the second group, hepatic venous [K] exceeded arterial [K] during the hyperkalemia, indicating loss of potassium by the liver, but was less than arterial [K] during the development of hypokalemia, indicating uptake of potassium by the liver at that time. In a third group, epinephrine (0.2 µg/kg/min) was infused locally into one femoral artery and plasma [K] was measured in the other femoral artery and both femoral veins. Venous [K] from the infused leg was reduced sooner and significantly more than was that from time opposite leg. These data suggest that epinephrine acts directly to increase the uptake of potassium by both liver and skeletal muscle and that the effects are mediated through adrenergic beta receptors.