Abstract: SA-PO0480
Potassium Depletion Impairs β-Intercalated Cell (β-IC)-Mediated Bicarbonate (HCO3-) Excretion
Session Information
- Top Trainee Posters - 3
November 08, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 01:06 PM - 01:12 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1101 Fluid, Electrolyte, and Acid-Base Disorders: Basic
Authors
- Ayasse, Niklas, Universitat Heidelberg Medizinische Fakultat Mannheim, Mannheim, BW, Germany
- Trans, Laura Woidemann, Aarhus Universitet Institut for Biomedicin, Aarhus, Central Denmark Region , Denmark
- Andersen, Jesper Frank, Aarhus Universitet Institut for Biomedicin, Aarhus, Central Denmark Region , Denmark
- Sorensen, Mads Vaarby, Aarhus Universitet Institut for Biomedicin, Aarhus, Central Denmark Region , Denmark
- Berg, Peder, Aarhus Universitet Institut for Biomedicin, Aarhus, Central Denmark Region , Denmark
- Leipziger, Jens G., Aarhus Universitet Institut for Biomedicin, Aarhus, Central Denmark Region , Denmark
Background
Hypokalemia often associates with metabolic alkalosis in the clinical setting. It is well-established that K+ depletion enhances renal net acid excretion and thus contributes to the generation of metabolic alkalosis. However, metabolic alkalosis only sustains if a maintaining factor impairs the kidneys’ great capacity to excrete excess HCO3-. β-intercalated cell function plays a pivotal role in the excretion of excess HCO3-, and we here hypothesize that K+ depletion impairs β-IC-mediated HCO3- excretion and thus contributes to the maintenance metabolic alkalosis.
Methods
β-IC function was assessed in C57/Bl6J mice of both sexes, subjected to either a control diet or a low K+ diet. The ability to activate β-IC-mediated HCO3- excretion, was tested in various ways: 1) 3-hour net base excretion was quantified after an oral HCO3- challenge in metabolic cages; 2) The urinary pH response to the application of secretin was measured in bladder catheterized mice; 3) The urinary pH response during acute respiratory alkalosis was measured in bladder catheterized mice during mechanical ventilation.
Results
1) An acute oral HCO3- load did not increase net base excretion in K+ deprived animals, opposite to what is seen in controls. 2) Secretin-induced acute urinary alkalization was evident in animals on control diet but absent in K+ deprived mice. 3) Acute respiratory alkalosis caused a rapid increase in urinary pH in animals on control diet but had no effect on urinary pH in in K+ deprived mice.
Conclusion
β-IC function is considerably impaired during K+ depletion indicating that the excretion of excess HCO3- is dependent on K+. During hypokalemia, impaired β-IC -mediated HCO3- excretion likely contributes to the maintenance of metabolic alkalosis.