title: Minor role of Cl- secretion in non-cystic fibrosis and cystic fibrosis human nasal epithelium.
abstract: Na+ and Cl- currents were studied in primary cultures of human nasal epithelium derived from non-cystic fibrosis (non-CF) and cystic fibrosis (CF) patients. We found that Na+ absorption dominates transepithelial transport and the Na+ current contains an amiloride-sensitive and amiloride-insensitive component. In non-CF tissue both components contribute about equally to the entire short-circuit current (ISC), whereas in CF tissues the major part of the current is amiloride-sensitive. Na+ removal reduced ISC to values close to zero. Several Cl- channel blockers were used to identify the remaining tiny Na+-independent current. Under unstimulated, physiological conditions in the presence of Cl- on both sides and amiloride on the apical side of the epithelium diphenylamine-2-carboxic acid (DPC), 4,4'-diisothiocyanatostilbene-2, 2'- disulfonic acid (DIDS) and 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB) failed to induce clearcut inhibition of ISC. cAMP as well as ATP did not affect ISC either in CF or in non-CF epithelia. Reduction of apical Cl- increased ISC and depolarized transepithelial potential; however, the observed increase was insensitive to DIDS, DPC and NPPB. From these data we conclude that Cl- conductances in primary cultures of human nasal epithelium derived from CF patients as well as from non-CF patients are present only in low numbers or do not contribute significantly to transepithelial ion transport.
authors.affiliation: CF Working Group Giessen, Justus Liebig University, Giessen, Belgium.
authors.forename: C
authors.initials: C
authors.lastname: Rückes-Nilges
authors.forename: U
authors.initials: U
authors.lastname: Weber
authors.forename: H
authors.initials: H
authors.lastname: Lindemann
authors.forename: G
authors.initials: G
authors.lastname: Münker
authors.forename: W
authors.initials: W
authors.lastname: Clauss
authors.forename: W M
authors.initials: WM
authors.lastname: Weber
mesh_terms: D017878:4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid / Q000494:pharmacology; D000255:Adenosine Triphosphate / Q000494:pharmacology; D000584:Amiloride / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002478:Cells, Cultured; D018118:Chloride Channels / Q000187:drug effects / Q000502:physiology; D002712:Chlorides / Q000378:metabolism*; D000242:Cyclic AMP / Q000494:pharmacology; D003550:Cystic Fibrosis / Q000503:physiopathology*; D006801:Humans; D008564:Membrane Potentials / Q000502:physiology; D009297:Nasal Mucosa / Q000378:metabolism* / Q000502:physiology / Q000503:physiopathology; D009579:Nitrobenzoates / Q000494:pharmacology; D012016:Reference Values; D012964:Sodium / Q000378:metabolism; D015222:Sodium Channels / Q000187:drug effects / Q000502:physiology; D062367:ortho-Aminobenzoates / Q000494:pharmacology
chemical_list: D002121:Calcium Channel Blockers; D018118:Chloride Channels; D002712:Chlorides; D009579:Nitrobenzoates; D015222:Sodium Channels; D062367:ortho-Aminobenzoates; C058176:5-nitro-2-(3-phenylpropylamino)benzoic acid; D000584:Amiloride; D000255:Adenosine Triphosphate; C001209:fenamic acid; D012964:Sodium; D000242:Cyclic AMP; D017878:4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid