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Impaired Renal Base Excretion in Secretin Receptor Knock-Out Mice During Prolonged Base-Loading
Tobias Jensen1, Jesper Frank Andersen1, Laura Woidemann Trans1
1Department of Biomedicine, Aarhus University, Aarhus, Denmark.
Acta Physiologica (Oxford, England)
|July 31, 2026
Summary
Secretin receptor (SCTR) loss impairs kidney base excretion during prolonged base-loading, worsening base accumulation. SCTR plays a key role in renal adaptation to acid-base balance.
Area of Science:
- Nephrology
- Endocrinology
- Physiology
Background:
- Secretin regulates renal adaptation to acute base excess by increasing pendrin-dependent HCO3- secretion.
- The role of secretin and its receptor in prolonged base-loading is not well understood.
Purpose of the Study:
- To investigate the role of the secretin receptor (SCTR) in renal adaptation to prolonged base-loading.
- To determine how SCTR influences pendrin function and acid-base balance during sustained base excess.
Main Methods:
- Utilized secretin receptor (SCTR) knockout (KO) and wild-type (WT) mice subjected to prolonged base-loading.
- Assessed urine and blood acid-base status, pendrin protein abundance and function, plasma secretin levels, and renal SCTR expression.
Main Results:
- SCTR KO mice showed reduced urine alkalization and increased blood base retention during base-loading.
- Pendrin function was significantly impaired in SCTR KO mice despite normal protein abundance.
- Plasma secretin and renal SCTR mRNA levels increased with base-loading and correlated with arterial HCO3-.
Conclusions:
- Loss of SCTR diminishes renal base excretion capacity and exacerbates systemic base accumulation.
- Plasma secretin and renal SCTR are modulated by acid-base intake, supporting their role in prolonged base excess regulation.
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