The sympathetic nervous system plays an important role in the control of plasma potassium levels. Administration of adrenaline or noradrenaline evokes, in the majority of mammal species a dual response: first a short transient hyperkalaemia, followed by a maintained hypokalaemia. Alpha 1- and alpha 2-adrenoceptors mediate the initial hyperkalaemia through the activation of hepatic Ca(2+)-dependent-K(+)-channels. Stimulation of beta 1- and beta 2-adrenoceptors induces the late hypokalaemia by stimulation of skeletal muscle Na(+)-K(+)-ATPase. Beta 3-adrenoceptor stimulation may also have an effect on plasma potassium control since administration of selective beta 3-adrenoceptor agonists induces a decrease in plasma potassium. The simultaneous infusion of phenyleprine (alpha-adrenoceptor agonist) and isoprenaline (beta-adrenoceptor agonist) increases plasma potassium levels: this effect is several times larger than the algebric summation of the changes in plasma potassium when each agent is infused separately, thus suggesting potentiation. The physiological (changes in cell volume and function secondary to changes in ion fluxes) and clinical implications (pathophysiological conditions with hypo or hyperkalaemia, hyperkalaemic periodic paralysis, ventricular arrythmias) of these findings are discussed.