Berg Peder, Svendsen Samuel L, Sorensen Mads Vaarby, Schreiber Rainer, Kunzelmann Karl, Leipziger Jens
Department of Biomedicine, Physiology, Health, Aarhus University, Aarhus, Denmark.
Department of Physiology, University of Regensburg, Regensburg, Germany.
J Physiol. 2021 Jun;599(12):3003-3011. doi: 10.1113/JP281285. Epub 2021 May 29.
This review summarizes the newly discovered molecular mechanism of secretin-stimulated urine HCO excretion and the role of cystic fibrosis transmembrane conductance regulator (CFTR) in renal HCO excretion. The secretin receptor is functionally expressed in the basolateral membrane of the HCO -secreting β-intercalated cells of the collecting duct. Here it activates a fast and efficient secretion of HCO into the urine serving to normalize metabolic alkalosis. The ability to acutely increase renal base excretion is entirely dependent on functional pendrin (SLC26A4) and CFTR, and both proteins localize to the apical membrane of the β-intercalated cells. In cystic fibrosis mice and patients, this function is absent or markedly reduced. We discuss that the alkaline tide, namely the transient urine alkalinity after a meal, has now received a clear physiological explanation.
本综述总结了新发现的促胰液素刺激尿液中碳酸氢根排泄的分子机制以及囊性纤维化跨膜传导调节因子（CFTR）在肾脏碳酸氢根排泄中的作用。促胰液素受体在集合管分泌碳酸氢根的β-闰细胞的基底外侧膜上功能性表达。在此，它激活向尿液中快速高效地分泌碳酸氢根，从而使代谢性碱中毒恢复正常。急性增加肾脏碱排泄的能力完全依赖于功能性的pendrin（SLC26A4）和CFTR，这两种蛋白均定位于β-闰细胞的顶端膜。在囊性纤维化小鼠和患者中，这种功能缺失或明显降低。我们讨论了碱潮，即餐后短暂的尿液碱化现象，现在已经得到了明确的生理学解释。
