imprint:
Springer Science and Business Media LLC, 2024
Published in:Pflügers Archiv - European Journal of Physiology
Language:
English
DOI:
10.1007/s00424-023-02899-5
ISSN:
0031-6768;
1432-2013
Origination:
Footnote:
Description:
<jats:title>Abstract</jats:title><jats:p>The kidney plays a crucial role in acid-base homeostasis. In the distal nephron, α-intercalated cells contribute to urinary acid (H<jats:sup>+</jats:sup>) secretion and β-intercalated cells accomplish urinary base (HCO<jats:sub>3</jats:sub><jats:sup>-</jats:sup>) secretion. β-intercalated cells regulate the acid base status through modulation of the apical Cl<jats:sup>-</jats:sup>/HCO<jats:sub>3</jats:sub><jats:sup>-</jats:sup> exchanger pendrin (SLC26A4) activity. In this review, we summarize and discuss our current knowledge of the physiological role of the renal transporter AE4 (SLC4A9). The AE4, as cation-dependent Cl<jats:sup>-</jats:sup>/HCO<jats:sub>3</jats:sub><jats:sup>-</jats:sup> exchanger, is exclusively expressed in the basolateral membrane of β-intercalated cells and is essential for the sensing of metabolic acid-base disturbances in mice, but not for renal sodium reabsorption and plasma volume control. Potential intracellular signaling pathways are discussed that might link basolateral acid-base sensing through the AE4 to apical pendrin activity.</jats:p>