Increase in serum potassium caused by beta-2 adrenergic blockade in terminal renal failure: absence of mediation by insulin or aldosterone.

To test the hypothesis that beta-blockade might impair potassium (K) tolerance in terminal renal failure we gave propranolol, and then atenolol, to a group of 12 clinically stable non-diabetic patients on chronic haemodialysis and on a constant diet containing approximately 50 mEq of K/day. Propranolol, 60 to 80 mg/day for 10 days induced a significant increase in predialysis serum K from 5.1 +/- 0.1 to 5.8 +/- 0.2 mEq/L (p less than 0.005). Atenolol (50 mg/day for 10 days) in the same group of patients did not produce a significant change in predialysis serum K (5.5 +/- 0.2 vs 5.2 +/- 0.2 mEq/L). Both propranolol and atenolol decreased heart rate but neither drug induced significant changes in plasma aldosterone, arterial pH, serum insulin or blood glucose. Thus in haemodialysis patients, beta-2 adrenergic blockade by propranolol is associated with a significant increase in serum K not mediated by pH, aldosterone or insulin, and probably due to inhibition of intracellular K uptake. Selective beta-1 adrenergic blockade by atenolol at low doses does not change serum K, and therefore, if indicated, cardioselective beta-blockers might be preferable to nonselective drugs in haemodialysis patients.