Increase in serum potassium caused by beta-2 adrenergic blockade in terminal renal failure: absence of mediation by insulin or aldosterone.
Increase in serum potassium caused by beta-2 adrenergic blockade in terminal renal failure: absence of mediation by insulin or aldosterone.
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终末期肾衰竭中β-2肾上腺素能阻滞引起的血清钾升高：缺乏胰岛素或醛固酮的调节。
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发表时间：
1983
期刊：
影响因子：
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通讯作者：
L. Revert
中科院分区：
文献类型：
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作者：
P. Arrizabalaga;J. Montoliu;A. MartínezVea;L. Andreu;J. LópezPedret;L. Revert
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.
