A moderate increase in serum potassium concentrations has been observed in several controlled clinical trials with beta-blockers. This increase cannot be explained by the retention of potassium in the organism, and is probably caused by the redistribution of potassium from intracellular to extracellular compartments. beta-adrenergic mechanisms seem to be concerned in the extrarenal handling of the potassium-load in man, presumably by inducing an increased uptake of potassium in muscular cells and liver cells. These beta-adrenergic mechanisms are probably of the beta 2-type. In theory there are several conditions in which it is important to have a defence against hyperkalaemia from exogenous or endogenous sources for example, during heavy physical exercise, after a potassium-rich meal, or after traumatic tissue damage. Available data indicate that non-selective beta-blockade increases serum potassium concentrations during and after heavy exercise and during coronary bypass. The clinical implications of these findings are unknown.