Aquatic organisms are often exposed to dramatic changes in salinity in the environment. Despite decades of research, many questions related to molecular and physiological mechanisms mediating sensing and adaptation to salinity stress remain unanswered. Here, responses of Vaucheria erythrospora, a turgor-regulating xanthophycean alga from an estuarine habitat, have been investigated. The role of ion uptake in turgor regulation was studied using a single cell pressure probe, microelectrode ion flux estimation (MIFE) technique and membrane potential (Em ) measurements. Turgor recovery was inhibited by Gd(3+) , tetraethylammonium chloride (TEA), verapamil and orthovanadate. A NaCl-induced shock rapidly depolarized the plasma membrane while an isotonic sorbitol treatment hyperpolarized it. Turgor recovery was critically dependent on the presence of Na(+) but not K(+) and Cl(-) in the incubation media. Na(+) uptake was strongly decreased by amiloride and changes in net Na(+) and H(+) fluxes were oppositely directed. This suggests active uptake of Na(+) in V. erythrospora mediated by an antiport Na(+) /H(+) system, functioning in the direction opposite to that of the SOS1 exchanger in higher plants. The alga also retains K(+) efficiently when exposed to high NaCl concentrations. Overall, this study provides insights into mechanisms enabling V. erythrospora to regulate turgor via ion movements during hyperosmotic stress.