Electroneutral sodium bicarbonate exchanger 1 (SLC4A8)

Electroneutral sodium bicarbonate exchanger 1 (SLC4A8) is a membrane transporter protein that mediates the exchange of sodium (Na+) and bicarbonate (HCO3^-) ions with chloride (Cl^-) in an electroneutral fashion. It has a stoichiometry of 2 HCO3^- and 1 Na^+ entering in exchange for 1 Cl^- exiting the cell[1][5]. SLC4A8 is highly expressed in the brain and testis, with moderate expression in the respiratory system and kidneys[1][4]. Its primary physiological roles include regulation of intracellular and presynaptic pH in neurons—particularly influencing synaptic glutamate release and neuronal excitability—as well as mediating a significant portion of Na+ reabsorption and fluid homeostasis in the renal cortical collecting duct[1][4]. The encoded protein is inhibited by DIDS and is relevant in genetic syndromes involving corneal dystrophy and deafness. SLC4A8 is part of the SLC4 family of bicarbonate transporters, all of which are central to pH regulation in cells throughout the body[2][5][3]. No major drugs, biomarkers, or specific therapeutic safety issues are established for SLC4A8 as of current knowledge, but research suggests importance in neurophysiology and kidney function[1][3][4].

Other names

Solute carrier family 4 member 8Sodium-driven chloride/bicarbonate exchangerNDCBENBC3k-NBC3Electroneutral Na(+)-driven Cl-HCO3 exchangerKIAA0739

Inhibition of exchanger function by DIDS, which blocks sodium and bicarbonate ion translocation[3]. Sodium, chloride, and bicarbonate ion exchange as core molecular mechanism.