A role for sodium-chloride cotransporters in the rapid regulation of ion uptake following acute environmental acidosis: new insights from the zebrafish model.

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.

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