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Chloride gradient is the driving force for ammonia/ammonium influx in human red blood cells

Ammonium/ammonia (AM) Rhesus transporters are expressed in tissues involved in AM generation, secretion and excretion, however, the physiological role of erythroid RhAG glycoprotein is not fully defined yet. AM concentration in red blood cells (RBCs) is approximately three times higher than in plasma and RBCs are the only blood cells that swell and lyse in isotonic ammonium (NH4+) buffer indicating that AM is transported inside the cell. Two main possible mechanisms of AM transport, including diffusion and active transport, are described, however, the real driving force for AM influx in RBCs is still under debate. RhAG and anion exchanger 1 (AE1, band 3, Cl‐/HCO3‐‐exchanger) form a structural complex in RBC membrane therefore we hypothesized that AE1 might be involved in AM influx in RBCs via the interplay with RhAG, and suggested that RhAG uses chloride (Cl‐) gradient mediated by AE1 to import NH4+ against the gradient.