Lymphocytic sodium and potassium pump function in Bartter's syndrome

Jest, Peder; Pedersen, K. E.; Klitgaard, N. A.; Thomsen, N.; Kjær, E.; Simonsen, Erik B.; Jacobsen, Jørgen

doi:10.1530/acta.0.1210061

Cited by 4 publications

(3 citation statements)

References 11 publications

(14 reference statements)

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“…Intracellular K+ concentration was measured only in a few studies, showing values in the lower part of the nor mal range [ 18,22,24] or frankly decreased [ 18,24], Only one of our patients had extremely decreased intracellular…”

Section: Discussionmentioning

confidence: 55%

“…After a widespread defect in the membrane sodium transport was postulated to cause the disease [ 12], several studies have been performed to identify it [13][14][15][16][17][18][19][20][21][22][23][24], In the majority of these studies, red blood cells have been uti lized as a cellular model to evaluate the activity of trans port systems. Although partial agreement seems to exist on the presence of high intracellular sodium concentra tion and increased passive permeability of cell membrane to sodium, the findings of all these studies are rather con troversial.…”

Section: Introductionmentioning

confidence: 99%

“…The absence of a well-defined picture could be par tially explained if we consider that different cellular mod els were used in some of these studies [24,35] and that remarkable differences exist between the methodologies that were employed. Moreover, it is difficult to distin guish the primary changes of membrane transport sys tems from those induced by the general electrolyte metab olism derangement which characterizes these patients.…”

mentioning

confidence: 99%

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Abnormalities of Erythrocyte Sodium Transport Systems in Bartter’s Syndrome

Sechi

Melis²,

Bartoli³

1992

Am J Nephrol

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The basic tubular alteration present in Bartter’s syndrome is still a subject of controversy. The possibility that a generalized defect in the transmembrane ion transport underlies the disease has been extensively investigated. Previous evaluations of cellular sodium metabolism in Bartter patients showed extremely variable findings. We have examined in the red blood cells of two patients with Bartter’s syndrome the intracellular Na⁺ and K⁺ concentrations, the activity of the ouabain-sensitive Na⁺/K⁺ pump, furosemide-sensitive Na⁺/K⁺ cotransport, Na⁺/Li⁺ countertransport and the rate constant of Na⁺ and K⁺ passive permeability. We have compared these values with those of healthy subjects and patients with chronic hypokalemia produced by conditions other than Bartter’s syndrome. Ouabain-sensitive Na⁺/K⁺ pump activity was decreased in both patients, whereas Na⁺/Li⁺ countertransport was activated. One of the patients also exhibited markedly decreased intraerythrocyte K⁺ concentration and decreased furosemide-sensitive Na⁺/K⁺ cotransport. The other had increased Na⁺/K⁺ cotransport activity and Na⁺ passive permeability. Intracellular Na⁺ and passive permeability to K⁺ were normal in both subjects. Neither oral potassium supplementation (100 mEq/day) nor indo-methacin treatment (150 mg/day) could correct these abnormalities. Our results are partially consistent with previous observations and indicate the existence of heterogenous abnormalities of erythrocyte sodium transport systems in patients with Bartter’s syndrome which are not a consequence of chronic hypokalemia.

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Section: Discussionmentioning

confidence: 55%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

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Abnormalities of Erythrocyte Sodium Transport Systems in Bartter’s Syndrome

Sechi

Melis²,

Bartoli³

1992

Am J Nephrol

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Angiotensin-converting enzyme inhibition as a therapeutic principle in Bartter's syndrome

Jest

Pedersen

Klitgaard

et al. 1991

Eur J Clin Pharmacol

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The effect of captopril has been investigated in four patients with Bartter's syndrome treated for 12 weeks. Baseline biochemistry showed normal serum aldosterone (mean 347 pmol.l-1) and a mean serum renin of 217 mU-l-1, and a considerable increase in serum renin during captopril treatment. Serum aldosterone decreased gradually during the study period to about half its initial value. The patients presented with a mean serum potassium of 2.5 mmol.l-1, which rose to 3.4 mmol.l-1 on captopril. Lymphocytes showed a substantial captopril-induced increase in intracellular sodium (from 15 to 22.5 mmol.l-1 on average), but no change in the potassium content. Captopril was well-tolerated. It may be an alternative to potassium-sparing diuretics for maintaining normal serum potassium levels in patients with Bartter's syndrome.

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