Bartter's syndrome is characterized by chronic hypokalaemia, activation of the renin-angiotensin system and normal blood pressure. To investigate whether a generalized disturbance of sodium-potassium pump function might be of pathogenetic importance, lymphocytic sodium-potassium homeostasis was examined in 5 patients suffering from Bartter's syndrome. Two of the patients were treated with potassium chloride supplementation, the others were without medical treatment when studied. All were severely hypokalemic (serum potassium 2.8 ± 0.24 mmol/l, mean ± sem). Lymphocyte sodium and potassium concentration (14.4 ± 0.37 and 94.4 ± 7.7 mmol/l, respectively), ouabain sensitive 22Na-efflux rate constant (2.68 ± 0.25 h −1), and absolute ouabain sensitive efflux rate (38.16 ± 4.2 mmol · I−1 · h−1) did not differ from matched controls. Ouabain binding capacity was 126900 ± 235000 sites/cell in the patients vs 50400 ± 17900 in controls (p <0.05). In conclusion, patients with Bartter's syndrome may have an intrinsic abnormal pump function, characterized by an increased pump density and a low cation turn-over rate per pump unit.