ArticleThe Journal of physiology2001
Oxygen-evoked Na+ transport in rat fetal distal lung epithelial cells.
Article in The Journal of physiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Endothelial ENaC as a repressor of oxidative stress and a guardian of lung capillary barrier function in bacterial and viral pneumonia.Frontiers in physiology · 2025Review
- Nadph oxidase regulates alveolar epithelial sodium channel activity and lung fluid balance in vivo via O⁻₂ signaling.American journal of physiology. Lung cellular and molecular physiology · 2012Article
- Oxygen regulation of the epithelial Na channel in the collecting duct.American journal of physiology. Renal physiology · 2011Article
- Control of HIF-1{alpha} and vascular signaling in fetal lung involves cross talk between mTORC1 and the FGF-10/FGFR2b/Spry2 airway branching periodicity clock.American journal of physiology. Lung cellular and molecular physiology · 2010Article
- Expression of ENaC subunits, chloride channels, and aquaporins in ovine fetal lung: ontogeny of expression and effects of altered fetal cortisol concentrations.American journal of physiology. Regulatory, integrative and comparative physiology · 2009Article
- Manipulation of gene expression by oxygen: a primer from bedside to bench.Pediatric research · 2009Review
- Redox regulation of epithelial sodium channels examined in alveolar type 1 and 2 cells patch-clamped in lung slice tissue.The Journal of biological chemistry · 2008Article
- Development of a lung slice preparation for recording ion channel activity in alveolar epithelial type I cells.Respiratory research · 2005Article
- A glucocorticoid-induced Na+ conductance in human airway epithelial cells identified by perforated patch recording.The Journal of physiology · 2004Article
- Science review: redox and oxygen-sensitive transcription factors in the regulation of oxidant-mediated lung injury: role for hypoxia-inducible factor-1alpha.Critical care (London, England) · 2003Review
- Hormonal modulation of Na(+) transport in rat fetal distal lung epithelial cells.The Journal of physiology · 2002Article
- Pulmonary oedema fluid induces non-alpha-ENaC-dependent Na(+) transport and fluid absorption in the distal lung.The Journal of physiology · 2002Article
- Oxygen-evoked changes in transcriptional activity of the 5'-flanking region of the human amiloride-sensitive sodium channel (alphaENaC) gene: role of nuclear factor kappaB.The Biochemical journal · 2002Article
- Oxygen-sensing mechanisms and the regulation of redox-responsive transcription factors in development and pathophysiology.Respiratory research · 2002Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Monolayer cultures of rat fetal distal lung epithelial (FDLE) cells generated larger spontaneous short circuit currents (ISC) when maintained (48 h) at neonatal alveolar PO2 (100 mmHg) than at fetal PO2 (23 mmHg). When cells were shifted between these atmospheres in order to impose a rise in PO2 equivalent to that seen at birth, no rise in ISC was seen after 6 h but the response was fully established by 24 h. Studies of basolaterally permeabilised cells revealed a small rise in apical Na+ conductance (GNa) 6 h after PO2 was raised but no further change had occurred by 24 h. A substantial rise was, however, seen after 48 h. Reporter gene assays showed that no activation of the -ENaC (epithelial Na+ channel -subunit) promoter was discernible 24 h after PO2 was raised but increased transcriptional activity was seen at 48 h. Studies of apically permeabilised cells showed that a small rise in Na+ pump capacity was evident 6 h after PO2 was raised and, in common with the rise in ISC, this effect was fully established by 24 h. The rise in ISC thus develops 6-24 h after PO2 is raised and is due, primarily, to increased Na+ pump capacity. The increase in GNa thus coincides with activation of the -ENaC promoter but these effects occur after the rise in ISC 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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.