Mechanisms of Bicarbonate Secretion: Lessons from the Airways
Mechanisms of Bicarbonate Secretion: Lessons from the Airways
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DOI：
10.1101/cshperspect.a015016
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发表时间：
2012-08-01
影响因子：
5.4
通讯作者：
Bridges, Robert J.
中科院分区：
文献类型：
--
作者：
Bridges, Robert J.
早期研究表明，气道细胞分泌HCO 3-响应cAMP介导的激动剂，并且在囊性纤维化（CF）中HCO 3-分泌受损。对Calu-3细胞（一种高表达CFTR的气道浆液模型）的研究也显示，当细胞被cAMP介导的激动剂刺激时，HCO 3-分泌。基底外侧膜hIK-1 K+通道的激活抑制HCO 3-分泌并刺激Cl-分泌。CFTR介导HCO 3-和Cl-穿过顶膜离开。HCO 3-进入基底外侧膜NBC或Cl-进入NKCC决定分泌哪种阴离子。这两种分泌阴离子之间的切换由hIK-1 K+通道的活性决定。
Early studies showed that airway cells secrete HCO3- in response to cAMP-mediated agonists and HCO3- secretionwas impaired in cystic fibrosis (CF). Studies with Calu-3 cells, an airway serous model with high expression of CFTR, also showthe secretion of HCO3- when cells are stimulated with cAMP-mediated agonists. Activation of basolateral membrane hIK-1 K+ channels inhibits HCO3- secretion and stimulates Cl- secretion. CFTR mediates the exit of both HCO3- and Cl- across the apical membrane. Entry of HCO3- on a basolateral membrane NBC or Cl- on the NKCC determines which anion is secreted. Switching between these two secreted anions is determined by the activity of hIK-1 K+ channels.