Lymphocytic sodium and potassium pump function in Bartter's syndrome

• Published in: Acta endocrinologica (Copenhagen) Vol. 121; no. 1; p. 61
• Main Authors: Jest, P, Pedersen, K E, Klitgaard, N A, Thomsen, N, Kjaer, E, Simonsen, E, Jacobsen, J G
• Format: Journal Article
• Language: English
• Published: Denmark 01-07-1989
• Subjects: Adult; Bartter Syndrome - blood; Bartter Syndrome - physiopathology; Female; Humans; Hyperaldosteronism - blood; Lymphocytes - metabolism; Male; Potassium - blood; Receptors, Drug - metabolism; Sodium - blood; Sodium-Potassium-Exchanging ATPase
• ISSN: 0001-5598
• DOI: 10.1530/acta.0.1210061

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), and absolute ouabain sensitive efflux rate (38.16 +/- 4.2 mmol l-1 h) did not differ from matched controls. Ouabain binding capacity was 126 900 +/- 23 500 sites/cell in patients vs 50 400 +/- 17 900 in controls (p less than 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.