Sodium coupled bicarbonate transporters in the kidney, an update

Sodium coupled bicarbonate transporters in the kidney, an update
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DOI:
10.1111/j.1365-201x.2004.01324.x
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发表时间:
2004-08-01
期刊:
ACTA PHYSIOLOGICA SCANDINAVICA
影响因子:
--
通讯作者:
Praetorius, J
Praetorius, J
中科院分区:
其他
文献类型:
--
作者:
Aalkjær, C;Frische, S;Praetorius, J

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最近已经克隆了五个编码钠依赖性碳酸氢盐转运蛋白的基因。这些基因属于SLC 4A基因家族。这篇简短的综述总结了我们对这些基因产物在肾脏的分布和功能的了解。最好的成员是SLC 4A 4和SLC 4A 7。SLC 4A 4编码一种产电Na+,HCO 3--协同转运蛋白(NBCe 1),存在于近端小管的基底外侧膜中,负责此处的碳酸氢盐流出,从而负责约80%的肾碳酸氢盐重吸收。SLC 4A 7编码电中性NBC(称为NBC 3和NBCn 1),其存在于粗升支和集合管远端部分的基底外侧以及连接和集合管中的闰细胞(顶部或基底外侧)中。在较厚的上升肢体中,NBCn 1可能对NH 4+重吸收很重要。SLCA 5编码一个产电NBC(称为NBC 4和NBCe 2),基于RT-PCR,其定位于肾脏,但确切定位有待于良好的抗体。这也是SLC 4A 8和SLC 4A 10基因产物的情况,它们是钠依赖性Cl-、HCO 3-交换剂。这一领域的最新进展大大增加了我们对复杂的肾脏酸碱状态调节的理解。
Recently five genes have been cloned, which code for sodium dependent bicarbonate transport proteins. These genes belong to the SLC4A gene family. This short review summarizes our knowledge of these gene products with respect to their renal distribution and function. The best characterized members are the SLC4A4 and SLC4A7. SLC4A4 codes for an electrogenic Na+, HCO3--cotransporter (NBCe1), which is present in the basolateral membranes of proximal tubules and is responsible for the bicarbonate efflux here, and thus about 80% of the renal bicarbonate reabsorption. SLC4A7 codes for an electroneutral NBC (called NBC3 and NBCn1), which is present basolaterally in the thick ascending limb and the distal part of the collecting ducts and in intercalated cells (either apically or basolaterally) in the connecting and collecting tubules. In the thick ascending limb NBCn1 may be important for NH4+ reabsorption. SLCA5 codes for an electrogenic NBC (called NBC4 and NBCe2), which based on RT-PCR is located to the kidney but the exact localization awaits a good antibody. This is also the case for the SLC4A8 and SLC4A10 gene products, which are sodium dependent Cl-, HCO3- exchangers. The recent development in this field substantially increases our understanding of the complex renal regulation of acid base status.