Pendrin and sodium channels: relevance to hypertension.
Pendrin and sodium channels: relevance to hypertension.
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发表时间：
2010-11
影响因子：
3.4
通讯作者：
S. Wall;Vladimir Pech
中科院分区：
文献类型：
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作者：
S. Wall;Vladimir Pech
肾间质细胞介导远曲小管（DCT）、连接小管（CNT）和皮质集合管（CCD）中OH-/H+当量和Cl-的分泌或吸收。在此过程中，它们调节酸碱平衡，血管容量和血压。在B型和非A型、非B型闰间细胞中，Cl-吸收和HCO 3-分泌通过顶端Na+非依赖性Cl-/HCO 3-交换剂pendrin完成。随着循环醛固酮或血管紧张素II的增加，pendrin丰度和功能上调。在不存在pendrin的情况下（Slc 26 a4（-/-）或pendrin缺失小鼠），醛固酮和血管紧张素II刺激的Cl-吸收减少，这减弱了对这些激素的血压反应。Pendrin还通过肾脏特异性机制调节醛固酮诱导的ENaC丰度和功能变化，该机制不涉及循环激素浓度的变化。相反，pendrin改变ENaC丰度和功能，至少部分地，通过改变管腔HCO 3-。因此，醛固酮和血管紧张素II调节血压的肾脏调节，部分是通过调节pendrin介导的Cl-吸收和ENaC介导的Na+吸收。本文综述了Cl-/HCO 3-交换体pendrin在肾脏血压调节中的作用。
Renal intercalated cells mediate the secretion or the absorption of OH-/H+ equivalents and Cl- in the distal convoluted tubule (DCT), the connecting tubule (CNT) and the cortical collecting duct (CCD). In so doing, they regulate acid-base balance, vascular volume and blood pressure. In type B and non-A, non-B intercalated cells, Cl- absorption and HCO3- secretion are accomplished through the apical Na+-independent Cl-/HCO3- exchanger, pendrin. With increased circulating aldosterone or angiotensin II, pendrin abundance and function are up-regulated. In the absence of pendrin (Slc26a4 (-/-) or pendrin null mice), aldosterone- and angiotensin II-stimulated Cl- absorption are reduced, which attenuates the blood pressure response to these hormones. Pendrin also modulates aldosterone-induced changes in ENaC abundance and function through a kidney-specific mechanism that does not involve changes in the concentration of a circulating hormone. Instead, pendrin changes ENaC abundance and function, at least in part, by altering luminal HCO3-. Thus, aldosterone and angiotensin II modulate the renal regulation of blood pressure, in part, by regulating pendrin-mediated Cl- absorption and ENaC-mediated Na+ absorption. This review summarizes the contribution of the Cl-/HCO3- exchanger, pendrin, in the renal regulation of blood pressure.