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Role of ENaC and of the Na/K pump on the Hypertonicity‐induced inhibition of Na Transport in Cystic Fibrosis Human Bronchial Epithelial Cells
Author(s) -
Rasgado-Flores Hector,
Ngansop Thierry,
Piennette Paul,
Gallegos Kevin,
Bridges Robert J
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.881.1
Subject(s) - epithelial sodium channel , ussing chamber , cystic fibrosis , chemistry , amiloride , cystic fibrosis transmembrane conductance regulator , ion transporter , apical membrane , sodium , transepithelial potential difference , intracellular , epithelium , biophysics , medicine , biochemistry , secretion , biology , membrane , pathology , organic chemistry
Hypertonic saline (HS) inhalation produces surprisingly long lasting benefits to Cystic Fibrosis (CF) patients. We have found that exposure to hypertonic challenge (HC) solutions produce long‐lasting inhibitions of the transepithelial short‐circuit current (ISC) in primary cultures of human bronchial epithelial (HBE) cells from CF donors. Aims To determine if the HS‐induced inhibition of ISC is due to inhibition of the epithelial Na+ channels (ENaC) and/or the basolateral Na/K ATPase. Methods HBE cells from CF were grown on Transwell inserts (air liquid interface) and were mounted on Ussing chambers to perform trans‐epithelial impedance analysis and measure transepithelial ISC, resistance (Rt), capacitance (Ct) and Conductance (Gt) The putative role of ENaC and of the Na/ATPase on the HC‐induced inhibition of the ISC was studied by permeabilizing the apical or basolateral membranes with Nystatin. Results i) Exposure to apical or basolateral HC‐NaCl or HC‐mannitol inhibited ISC. ii) Exposure to HC‐solutions induced cell shrinkage as indicated by a reduction in CT.; iii) Neither activity of the Na/K ATPase nor the ENaC was absolutely required for the HC‐induced inhibition of ISC. Conclusions Cell shrinkage, together with a likely increase in the intracellular Na+ concentration inhibit transepithelial Na transport (ISC). Both, the ENaC and the Na/K ATPase play a role in this inhibition.