Cardiovascular performance was studied in 18 α‐chloralose anaesthetized pigs when arterial potassium ([K+]a) was raised to levels observed in heavy exercise. The effects of hyperkalaemia were then studied during cardiac sympathetic nerve stimulation or during an infusion of noradrenaline. Elevation of [K+]aup toca.10 mM caused a progressive decline in cardiovascular performance. However, right cardiac sympathetic nerve stimulation elevated all cardiovascular parameters in the presence of raised [K+]aand offset the negative cardiac effects of hyperkalaemia. Electrical pacing of the right atrium to heart rates (HRs) equivalent to those observed during right cardiac sympathetic nerve stimulation did not offset the depressive effects of hyperkalaemia and, indeed, hastened the decline in cardiovascular performance. Infusion of noradrenaline (1m̀g kg min‐1i. v.) during hyperkalaemia caused an increase in all cardiovascular parameters similar to that seen during sympathetic nerve stimulation. After propranolol (0.5 mg kg‐1i. v.), sympathetic nerve stimulation slightly increased HR, systolic blood pressure (SBP) and dP/dtmax. Elevation of [K+]aoccurred more rapidly after propranolol, but the heart was still protected from hyperkalaemia during cardiac sympathetic stimulation. Infusion of noradrenaline elicited arrhythmias in six pigs. Infusion of KCI reduced the incidence of arrhythmias and in some cases abolished them. These findings may be related to how the heart is protected from exercise‐induced changes in potassium and catec