We have investigated volume-activated taurine transport and ultrastructural swelling response of sea bass gill cells in culture, assuming that euryhaline fish may have developed particularly efficient mechanisms of salinity adaptation. In vivo, when sea basses were progressively transferred from seawater to freshwater, we observed a decrease in blood osmotic pressure. When gill cells in culture were subjected to 30 % hypotonic shock, we observed a 5-fold stimulation of [³H]taurine efflux. This transport was reduced by various anion channel inhibitors with the following efficiency: NPPB>niflumic acid>DIDS=DPC. The hypotonic shock produced a 5-fold stimulation of apical taurine efflux, whereas basolateral exit was 25 times higher. Experiments using ionomycin, removal of extracellular calcium, thapsigargin or BAPTA-AM suggested that taurine transport was regulated by external calcium. The inhibitory effects of lanthanum and streptomycin support Ca⁺⁺ entry through mecano-sensitive Ca⁺⁺ channels. Branchial cells also showed hypotonically-activated anionic currents sensitive to DIDS and NPPB. Similar pharmacology and time course suggested the potential existence of a common pathway for osmosensitive taurine and Cl^- efflux through VSOAC channels. Immunochemistry labelling showed that endogenous taurine was present in cultured gill cells. A three-dimensional structure study revealed that respiratory gill cells began to swell only 15 s after hypoosmotic shock. Apical microridges showed membrane outfoldings: the cell surface became smoother with a progressive disappearance of ridges. Therefore, osmotic swelling may not actually induce membrane stretch per se, inasmuch as the microridges may provide a reserve of surface area. This work demonstrates mechanisms of functional and morphological plasticity of branchial cells during osmotic stress.