SLC₄A11, a member of the SLC₄ family of bicarbonate transporters, is a widely expressed integral membrane protein, abundant in kidney and cornea. Mutations of SLC₄A11 cause some cases of the blinding corneal dystrophies, congenital hereditary endothelial dystrophy and Fuchs endothelial corneal dystrophy. These diseases are marked by fluid accumulation in the corneal stroma, secondary to defective fluid reabsorption by the corneal endothelium. The role of SLC₄A11 in these corneal dystrophies is not firmly established, as SLC₄A11 function remains unclear. To clarify the normal function(s) of SLC₄A11, we characterized the protein following expression in the simple, low-background, expression system, X. laevis oocytes. Since plant and fungal SLC₄A11 orthologs transport borate, we measured cell swelling associated with accumulation of solute, borate. The plant water/borate transporter, Nip5;1, manifested borate transport, whereas human SLC₄A11 did not. SLC₄A11 supported osmotically-driven water accumulation that was electroneutral and Na⁺-independent. Studies in oocytes and HEK293 cells could not detect Na⁺-coupled HCO₃^- transport or Cl^-/HCO₃^- exchange by SLC₄A11. SLC₄A11 mediated electroneutral NH₃ transport in oocytes. Voltage-dependent OH^- or H⁺ movement was not measurable in SLC₄A11 expressing oocytes, but SLC₄A11-expressing HEK293 cells manifested low level cytosolic acidification at baseline. In mammalian cells, but not oocytes, OH^-/H⁺ conductance may arise when SLC₄A11 activates another protein or itself is activated by another protein. These data argue against a role of human SLC₄A11 in bicarbonate or borate transport. This work provides additional support for water and ammonia transport by SLC₄A11. When expressed in oocytes, SLC₄A11 transported NH₃, not NH₃/H⁺.