Epinephrine and potassium homeostasis

Abstract

The effect of epinephrine on potassium metabolism was examined in six subjects. Each subject participated in four studies as follows: (1) potassium chloride infusion (0.75 mEq/kg, i.v.) given over 2 hours, (2) epinephrine (0.05 μg/kg.min) plus potassium chloride, (3) propranolol (1.43 μg/kg.min) plus epinephrine plus potassium chloride, and (4) propranolol plus potassium chloride. The epinephrine infusion with potassium chloride led to a marked improvement in potassium tolerance, which was due to a greater than twofold increase in the extrarenal disposal of potassium (P <0.001). The enhancing effect of epinephrine on extrarenal potassium uptake was completely reversed with the beta-blocking agent propranolol. When propranolol alone was infused with potassium chloride, a significant decrease in the extrarenal disposal of potassium was observed. When potassium chloride was infused alone, 47% of the administered potassium load was excreted in the urine. Epinephrine infusion with potassium chloride markedly inhibited the urinary excretion of potassium (UKV) to rates that were actually below the basal potassium excretion rate (P <0.001). Propranolol almost completely reversed this effect of epinephrine on UKV, and when propranolol was infused alone, and enhancement in UKV (P <0.005) was observed. Insulin adds only a minor contribution to the enhancing effect of epinephrine on extrarenal potassium disposal and does not contribute at all to the inhibitory effect of epinephrine on renal potassium excretion. These results demonstrate that epinephrine ameliorates the rise in plasma potassium concentration following potassium chloride infusion. Because none of the infused potassium was excreted during the 4-hour study period, the improvement in potassium tolerance must result from an enhancement in extrarenal potassium disposal. The ability of propranolol to reverse both the extrarenal and renal effects indicates that the action of epinephrine is mediated via stimulation of the beta receptor.