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Oxygen‐evoked Na + transport in rat fetal distal lung epithelial cells
Author(s) -
Baines D. L.,
Ramminger S. J.,
Collett A.,
Haddad J. J. E.,
Best O. G.,
Land S. C.,
Olver R. E.,
Wilson S. M.
Publication year - 2001
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.2001.0105g.x
Subject(s) - epithelial sodium channel , fetus , chemistry , oxygen , microbiology and biotechnology , lung , conductance , biophysics , biology , medicine , sodium , genetics , pregnancy , organic chemistry , mathematics , combinatorics
1 Monolayer cultures of rat fetal distal lung epithelial (FDLE) cells generated larger spontaneous short circuit currents ( I SC ) when maintained (48 h) at neonatal alveolar P O2 (100 mmHg) than at fetal P O2 (23 mmHg). When cells were shifted between these atmospheres in order to impose a rise in P O2 equivalent to that seen at birth, no rise in I SC was seen after 6 h but the response was fully established by 24 h. 2 Studies of basolaterally permeabilised cells revealed a small rise in apical Na + conductance ( G Na ) 6 h after P O2 was raised but no further change had occurred by 24 h. A substantial rise was, however, seen after 48 h. 3 Reporter gene assays showed that no activation of the α ‐ENaC (epithelial Na + channel α ‐subunit) promoter was discernible 24 h after P O2 was raised but increased transcriptional activity was seen at 48 h. 4 Studies of apically permeabilised cells showed that a small rise in Na + pump capacity was evident 6 h after P O2 was raised and, in common with the rise in I SC , this effect was fully established by 24 h. The rise in I SC thus develops 6‐24 h after P O2 is raised and is due, primarily, to increased Na + pump capacity. 5 The increase in G Na thus coincides with activation of the α ‐ENaC promoter but these effects occur after the rise in I SC is fully established and so cannot underlie this physiological response. The increased transcription may be an adaptation to increased Na + transport and not its cause.