Intracellular potential measurements of confluent monolayers of cultured bovine corneal endothelial cells were used to define passive ion transport processes in these cells. Previous studies (Jentsch et al. J. Membr. Biol. 78:103 (1984); Jentsch et al. J.Membr. Biol 81: 189 (1984)) have provided the experimental“Basis for a cellular model, in which bicarbonate entry across the basolateral membrane is indirectly driven by a Na+/H+-exchanger, which is inhibitable by amiloride (1mM). Bicarbonate and sodium should leave the cell via an electrogenic bicarbonate sodium cotransport, which is inhibitable by the disulfonic stilbene derivates SITS or DIDS. Tnis model is also consistent with results from transendothelial studies.In this paper, we briefly review the evidence we have obtained for this model and demonstrate, that the electrical response to sodium (depolarization upon Na -removal) is neither due to an inhibition of Na+/K -ATPase nor explainable in terms of changes in K -conductance. This is concluded from the observation of these responses in the presence of ouabain (10−4M) or barium (ImM).