Impairment of beta 2-adrenoceptor-stimulated potassium uptake in end-stage renal disease.

An abnormality of extrarenal mechanisms is believed to contribute importantly to the impaired potassium homeostasis in chronic renal failure. We evaluated the plasma potassium response to inhalation of albuterol, a beta 2 agonist, in eight patients who had end-stage renal disease and who were undergoing chronic hemodialysis and in eight control subjects. The purpose was to assess if an abnormality of the beta 2 adrenoceptor mechanism is present in uremia. The maximal decrement in plasma potassium concentration in the patients (0.12 +/- 0.04 mEq/L) was significantly less than that of the control subjects (0.30 +/- 0.05). Furthermore, the final plasma potassium concentration slightly exceeded baseline in the patients but was significantly reduced in controls, leading to the conclusion that an abnormal responsiveness of the beta 2 adrenoceptor may contribute to the impaired potassium tolerance found in patients who have end-stage renal disease.