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Lymphocytic sodium and potassium pump function in Bartter's syndrome.
P Jest1, K E Pedersen, N A Klitgaard
1Department of Clinical Chemistry, Odense University Hospital, Denmark.
Acta Endocrinologica
|July 1, 1989
Summary
Patients with Bartter's syndrome exhibit abnormal sodium-potassium pump function in lymphocytes. This involves increased pump numbers but reduced efficiency, contributing to the condition's pathogenesis.
Area of Science:
- Nephrology
- Cellular Physiology
- Molecular Medicine
Background:
- Bartter's syndrome presents with chronic hypokalemia and renin-angiotensin system activation.
- The role of sodium-potassium pump function in Bartter's syndrome pathogenesis is not fully understood.
Purpose of the Study:
- To investigate lymphocytic sodium-potassium homeostasis in patients with Bartter's syndrome.
- To determine if altered sodium-potassium pump function contributes to the pathophysiology of Bartter's syndrome.
Main Methods:
- Examined sodium-potassium homeostasis in lymphocytes from 5 Bartter's syndrome patients and matched controls.
- Measured lymphocyte sodium and potassium concentrations, and ouabain-sensitive 22Na-efflux.
- Quantified ouabain binding capacity to assess sodium-potassium pump density.
Main Results:
- Lymphocyte sodium and potassium concentrations and efflux rates were similar between patients and controls.
- Patients with Bartter's syndrome showed significantly higher ouabain binding capacity (increased pump density).
- A lower cation turnover rate per pump unit was observed in Bartter's syndrome patients.
Conclusions:
- Bartter's syndrome is associated with an intrinsic abnormality in sodium-potassium pump function.
- This abnormality is characterized by increased pump numbers and decreased individual pump efficiency.
- These findings suggest a novel pathogenetic mechanism in Bartter's syndrome involving cellular ion transport.