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首页> 美国卫生研究院文献>American Journal of Physiology - Cell Physiology >A role for sodium-chloride cotransporters in the rapid regulation of ion uptake following acute environmental acidosis: new insights from the zebrafish model
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A role for sodium-chloride cotransporters in the rapid regulation of ion uptake following acute environmental acidosis: new insights from the zebrafish model

机译：氯化钠共转运蛋白在急性环境酸中毒后快速调节离子吸收中的作用：斑马鱼模型的新见解

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摘要

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.
机译：在斑马鱼斑马鱼Danio rerio中研究了急性暴露于酸性水对Na + 和Cl -稳态的影响及其补偿调节的机制。暴露于酸性水（pH 4.0；对照pH 7.6）中2 h显着降低了Na + 的吸收和整个Na + 的含量。尽管如此，在预先暴露于酸性水中但在对照水中测定的鱼中，Na + 的吸收能力显着增加。根据Na + 选择性染料钠绿的积累，两种离子细胞亚型在暴露于酸性水中后表现出细胞内Na + 富集：H + -ATPase富集（HR）细胞，其共表达Na + / H + 交换异构体3b（NHE3b）和非HR细胞群体。在经历Na + -Cl -共转运蛋白（NCC）敲低的鱼中，我们观察到后一种细胞类型中没有钠绿蓄积，表明非HR细胞是NCC细胞。消除表达NHE3b的HR细胞并不能阻止酸暴露后Na + 摄取的增加。另一方面，当酸性水中富含Na + 和Cl -而不是Na时，Na + 的摄取被取消。仅 + ，表明酸暴露后升高的Na + 摄取与Cl -的补偿性调节有关。进一步的检查表明，急性酸暴露还降低了全身Cl -的水平，并增加了Cl -的吸收能力。此外，敲除NCC可以防止暴露于酸性水后Na + 和Cl -的吸收增加。总之，本研究的结果揭示了NCC在急性酸中毒后在Na + 和Cl -摄取的补偿性调节中的新作用。

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