Potassium chloride (96 mmol potassium/day) in the form of 12 Slow K tablets/day in 10 patients on an intake of 150 mmol sodium and 80 mmol potassium produced a cumulative sodium loss of 110 mmol by the 12th day of potassium supplementation. At the same time there was attenuation of the expected increase in plasma renin activity appropriate for such a sodium loss. The lack of rise in plasma renin activity and hence angiotensin II combined with sodium loss may account at least in part for the observed blood pressure fall. No change in ouabain-sensitive or total white cell sodium efflux rate constant was found. An effect of an increase in plasma potassium on the sodium pump cannot be excluded as the white cell sodium efflux rate constant was measured in a fixed external potassium concentration. There was no evidence from plasma noradrenaline measurements that increasing potassium intake reduces sympathetic activity in the resting state.