The effects of acute exposure to acidic water on Na and Cl homeostasis， and the mechanisms underlying their compensatory regulation， were investigated in the larval zebrafish Danio rerio Exposure to acidic water (pH 4.0; control pH 7.6) for 2 h significantly reduced Na uptake and whole body Na content. Nevertheless， the capacity for Na uptake was substantially increased in fish preexposed to acidic water but measured in control water. Based on the accumulation of the Na-selective dye， Sodium Green， two ionocyte subtypes exhibited intracellular Na enrichment after preexposure to acidic water: H-ATPase rich (HR) cells， which coexpress the Na/H exchanger isoform 3b (NHE3b)， and a non-HR cell population. In fish experiencing Na-Cl cotransporter (NCC) knockdown， we observed no Sodium Green accumulation in the latter cell type， suggesting the non-HR cells were NCC cells. Elimination of NHE3b-expressing HR cells did not prevent the increased Na uptake following acid exposure. On the other hand， the increased Na uptake was abolished when the acidic water was enriched with Na and Cl， but not with Na only， indicating that the elevated Na uptake after acid exposure was associated with the compensatory regulation of Cl Further examinations demonstrated that acute acid exposure also reduced whole body Cl levels and increased the capacity for Cl uptake. Moreover， knockdown of NCC prevented the increased uptake of both Na and Cl after exposure to acidic water. Together， the results of the present study revealed a novel role of NCC in the compensatory regulation of Na and Cl uptake following acute acidosis.