CL- REGULATION OF A CA2-ACTIVATED NONSELECTIVE CATION CHANNEL IN BETA-AGONIST-TREATED FETAL DISTAL LUNG EPITHELIUM()

Citation
H. Tohda et al., CL- REGULATION OF A CA2-ACTIVATED NONSELECTIVE CATION CHANNEL IN BETA-AGONIST-TREATED FETAL DISTAL LUNG EPITHELIUM(), The American journal of physiology, 266(1), 1994, pp. 30000104-30000109
Citations number
39
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Physiology
ISSN journal
0002-9513
Volume
266
Issue
1
Year of publication
1994
Part
1
Pages
30000104 - 30000109
Database
ISI
SICI code
0002-9513(1994)266:1<30000104:CROACN>2.0.ZU;2-Q
Abstract
Nonselective cation (NSC) channels have been identified in the apical membrane of fetal distal lung epithelium (FDLE). However, their physio logical role in Na+ transport is uncertain. Because terbutaline, a bet a(2)-agonist, increases Na+ transport by FDLE, we studied its effect a nd selected signal transduction mechanisms on NSC channel activity. Us ing patch-clamp and single-cell imaging techniques, we found that terb utaline activated the NSC channel by 1) increasing its sensitivity to cytosolic Ca2+ concentration ([Ca2+](c)) by 100- to 1,000-fold, 2) inc reasing [Ca2+](c) from 35 nM to 3.3 mu M, 3) producing a dependency of the NSC channel activity on the cytosolic Cl- concentration ([Cl-](c) ) at a physiological [Ca2+](c), and 4) inducing a reduction in the [Cl -](c) from 45 to 25 mM, which directly activates the beta(2)-treated N SC channel. These observations indicate that a beta(2)-agonist physiol ogically activates an amiloride-blockable NSC channel in FDLE through an increase in its sensitivity to [Ca2+](c), resulting in the developm ent of a [Cl-](c) dependency at a physiological [Ca2+](c), associated with both an increase in [Ca2+](c) and a reduction in [Cl-](c). A deve lopment of the [Cl-](c) dependency and a reduction in [Cl-](c) act as a second messenger of the beta-agonist signal transduction pathway in this Na+-transporting epithelium.