Department of Physiology and Biophysics, Rosalind Franklin University of Medicine and Sciences, North Chicago, IL 60064, USA.
Cold Spring Harb Perspect Med. 2012 Aug 1;2(8):a015016. doi: 10.1101/cshperspect.a015016.
Early studies showed that airway cells secrete HCO(3)(-) in response to cAMP-mediated agonists and HCO(3)(-) secretion was impaired in cystic fibrosis (CF). Studies with Calu-3 cells, an airway serous model with high expression of CFTR, also show the secretion of HCO(3)(-) when cells are stimulated with cAMP-mediated agonists. Activation of basolateral membrane hIK-1 K(+) channels inhibits HCO(3)(-) secretion and stimulates Cl(-) secretion. CFTR mediates the exit of both HCO(3)(-) and Cl(-) across the apical membrane. Entry of HCO(3)(-) 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.
早期研究表明，气道细胞在 cAMP 介导的激动剂的作用下分泌 HCO(3)(-)，囊性纤维化 (CF) 中 HCO(3)(-)的分泌受损。用 Calu-3 细胞进行的研究也表明，当用 cAMP 介导的激动剂刺激细胞时，HCO(3)(-)也会分泌。基底外侧膜 hIK-1 K(+)通道的激活抑制 HCO(3)(-)的分泌并刺激 Cl(-)的分泌。CFTR 介导 HCO(3)(-)和 Cl(-)穿过顶膜的共同外排。HCO(3)(-)进入基底外侧膜 NBC 或 Cl(-)进入 NKCC 决定了哪种阴离子被分泌。这两种分泌的阴离子之间的转换取决于 hIK-1 K(+)通道的活性。
