ArticleAmerican journal of physiology. Renal physiology2013
Fulvene-5 inhibition of Nadph oxidases attenuates activation of epithelial sodium channels in A6 distal nephron cells.
Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 21 citations in OpenAlex.
- Ligand-Controlled Chemoselectivity in the Rhodium-Catalyzed Synthesis of Pentafulvenes via (2 + 2 + 1) Alkyne Cyclotrimerization.Angewandte Chemie (International ed. in English) · 2025Article
- Review
- Epithelial NaComprehensive Physiology · 2024Review
- NOXA1-dependent NADPH oxidase 1 signaling mediates angiotensin II activation of the epithelial sodium channel.American journal of physiology. Renal physiology · 2022Article
- Effects of reactive oxygen species on renal tubular transport.American journal of physiology. Renal physiology · 2019Review
- The role of stretch-activated ion channels in acute respiratory distress syndrome: finally a new target?American journal of physiology. Lung cellular and molecular physiology · 2016Review
- Hydrogen Peroxide and Sodium Transport in the Lung and Kidney.BioMed research international · 2016Review
- Reactive oxygen species as important determinants of medullary flow, sodium excretion, and hypertension.American journal of physiology. Renal physiology · 2015Review
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Authors and funding
8 authors at 2 institutions in 1 country.
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Abstract
Nadph oxidase 4 is an important cellular source of reactive oxygen species (ROS) generation in the kidney. Novel antioxidant drugs, such as Nox4 inhibitor compounds, are being developed. There is, however, very little experimental evidence for the biological role and regulation of Nadph oxidase isoforms in the kidney. Herein, we show that Fulvene-5 is an effective inhibitor of Nox-generated ROS and report the role of Nox isoforms in activating epithelial sodium channels (ENaC) in A6 distal nephron cells via oxidant signaling and cell stretch activation. Using single-channel patch-clamp analysis, we report that Fulvene-5 blocked the increase in ENaC activity that is typically observed with H2O2 treatment of A6 cells: average ENaC NPo values decreased from a baseline level of 1.04 ± 0.18 (means ± SE) to 0.25 ± 0.08 following Fulvene-5 treatment. H2O2 treatment failed to increase ENaC activity in the presence of Fulvene-5. Moreover, Fulvene-5 treatment of A6 cells blocked the osmotic cell stretch response of A6 cells, indicating that stretch activation of Nox-derived ROS plays an important role in ENaC regulation. Together, these findings indicate that Fulvene-5, and perhaps other classes of antioxidant inhibitors, may represent a novel class of compounds useful for the treatment of pathological disorders stemming from inappropriate ion channel activity, such as hypertension.
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Registered trials
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