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首页> 外文期刊>American Journal of Physiology >Basolateral ammonium transport by the mouse inner medullary collecting duct cell (mIMCD-3).
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Basolateral ammonium transport by the mouse inner medullary collecting duct cell (mIMCD-3).

机译：基底外侧铵通过小鼠内髓收集管细胞（mIMCD-3）转运。

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The renal collecting duct is the primary site for the ammonia secretion necessary for acid-base homeostasis. Recent studies have identified the presence of putative ammonia transporters in the collecting duct, but whether the collecting duct has transporter-mediated ammonia transport is unknown. The purpose of this study was to examine basolateral ammonia transport in the mouse collecting duct cell (mIMCD-3). To examine mIMCD-3 basolateral ammonia transport, we used cells grown to confluence on permeable support membranes and quantified basolateral uptake of the radiolabeled ammonia analog [14C]methylammonia ([14C]MA). mIMCD-3 cell basolateral MA transport exhibited both diffusive and transporter-mediated components. Transporter-mediated uptake exhibited a Km for MA of 4.6 +/- 0.2 mM, exceeded diffusive uptake at MA concentrations below 7.0 +/- 1.8 mM, and was competitively inhibited by ammonia with a Ki of 2.1 +/- 0.6 mM. Transporter-mediated uptake was not altered by inhibitors of Na+-K+-ATPase, Na+-K+-2Cl(-) cotransporter, K+ channels or KCC proteins, by excess potassium, by extracellular sodium or potassium removal or by varying membrane potential, suggesting the presence of a novel, electroneutral ammonia-MA transport mechanism. Increasing the outwardly directed transmembrane H+ gradient increased transport activity by increasing Vmax. Finally, mIMCD-3 cells express mRNA and protein for the putative ammonia transporter Rh B-glycoprotein (RhBG), and they exhibit basolateral RhBG immunoreactivity. We conclude that mIMCD-3 cells express a basolateral electroneutral NH4+/H+ exchange activity that may be mediated by RhBG.
机译：肾收集管是酸碱稳态所必需的氨分泌的主要部位。最近的研究已经确定在收集管中存在假定的氨转运蛋白，但是尚不清楚收集管是否具有由转运蛋白介导的氨转运。这项研究的目的是检查小鼠收集导管细胞（mIMCD-3）中基底外侧氨的转运。为了检查mIMCD-3基底外侧氨的转运，我们使用了生长在可渗透支撑膜上汇合的细胞，并定量了放射性标记的氨类似物[14C]甲基氨（[14C] MA）的基底外侧摄取。 mIMCD-3细胞基底外侧MA转运同时表现出扩散和转运蛋白介导的成分。转运蛋白介导的吸收表现出MA的Km为4.6 +/- 0.2 mM，在MA浓度低于7.0 +/- 1.8 mM时超过了扩散吸收，并且被氨竞争性抑制，Ki为2.1 +/- 0.6 mM。 Na + -K + -ATPase，Na + -K + -2Cl（-）共转运蛋白，K +通道或KCC蛋白的抑制剂，过量的钾，细胞外钠或钾的去除或膜电位的变化都不会改变转运蛋白介导的摄取。新型电中性氨-MA转运机制的存在。增加向外的跨膜H +梯度可通过增加Vmax来增加转运活性。最后，mIMCD-3细胞表达假定的氨转运蛋白Rh B-糖蛋白（RhBG）的mRNA和蛋白质，并表现出基底外侧RhBG免疫反应性。我们得出结论，mIMCD-3细胞表达可能由RhBG介导的基底外侧电中性NH4 + / H +交换活性。

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