ArticleThe Journal of biological chemistry2005
Superoxide anions are involved in mediating the effect of low K intake on c-Src expression and renal K secretion in the cortical collecting duct.
Article in The Journal of biological chemistry, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 47 citations in OpenAlex.
- Mechanistic target of rapamycin complex-1 plays a role in inhibiting kidney KAmerican journal of physiology. Renal physiology · 2026Article
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- GDF15, an Emerging Player in Renal Physiology and Pathophysiology.International journal of molecular sciences · 2024Review
- Angiotensin II acts through Rac1 to upregulate pendrin: role of NADPH oxidase.American journal of physiology. Renal physiology · 2024Article
- Kir4.2 mediates proximal potassium effects on glutaminase activity and kidney injury.Cell reports · 2022Article
- (Pro)renin receptor activation increases profibrotic markers and fibroblast-like phenotype through MAPK-dependent ROS formation in mouse renal collecting duct cells.Clinical and experimental pharmacology & physiology · 2017Article
- PGFAmerican journal of physiology. Renal physiology · 2017Article
- Effects of Reactive Oxygen Species on Tubular Transport along the Nephron.Antioxidants (Basel, Switzerland) · 2017Review
- MicroRNA-194 (miR-194) regulates ROMK channel activity by targeting intersectin 1.American journal of physiology. Renal physiology · 2014Article
- NADPH oxidases, reactive oxygen species, and the kidney: friend and foe.Journal of the American Society of Nephrology : JASN · 2013Review
- Inhibition of ROMK channels by low extracellular K+ and oxidative stress.American journal of physiology. Renal physiology · 2013Article
- MicroRNA 802 stimulates ROMK channels by suppressing caveolin-1.Journal of the American Society of Nephrology : JASN · 2011Article
- NAD(P)H oxidase and renal epithelial ion transport.American journal of physiology. Regulatory, integrative and comparative physiology · 2011Review
- Decrease in dietary K intake stimulates the generation of superoxide anions in the kidney and inhibits K secretory channels in the CCD.American journal of physiology. Renal physiology · 2010Article
- POSH stimulates the ubiquitination and the clathrin-independent endocytosis of ROMK1 channels.The Journal of biological chemistry · 2009Article
- Inhibition of angiotensin type 1 receptor impairs renal ability of K conservation in response to K restriction.American journal of physiology. Renal physiology · 2009Article
- Recent advances in understanding integrative control of potassium homeostasis.Annual review of physiology · 2009Review
- Chemistry and antihypertensive effects of tempol and other nitroxides.Pharmacological reviews · 2008Review
- K restriction inhibits protein phosphatase 2B (PP2B) and suppression of PP2B decreases ROMK channel activity in the CCD.American journal of physiology. Cell physiology · 2008Article
- Role of gp91phox -containing NADPH oxidase in mediating the effect of K restriction on ROMK channels and renal K excretion.Journal of the American Society of Nephrology : JASN · 2007Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
We previously demonstrated that low K intake stimulated the expression of c-Src and that stimulation of protein tyrosine kinase inhibited ROMK channel activity (Wei, Y., Bloom, P., Lin, D. H., Gu, R. M., and Wang, W. H. (2001) Am. J. Physiol. 281, F206-F212). Decreases in dietary K content significantly increased O(2)(-) levels and the phosphorylation of c-Jun, a transcription factor, in renal cortex and outer medulla. The role of O(2)(-) and related products such as H(2)O(2) in stimulating the expression of protein tyrosine kinase is suggested by the observation that addition of 50-200 microm H(2)O(2) increased the phosphorylation of c-Jun and the expression of c-Src in M1 cells, a mouse collecting duct principal cell line. The effect of H(2)O(2) on c-Src expression was completely abolished with cyclohexamide or actinomycin D. The treatment of animals on a K-deficient (KD) diet with tempol for 7 days significantly decreased the production of O(2)(-), c-Jun phosphorylation, and c-Src expression. Moreover, low K intake decreased the activity of ROMK-like small conductance channels from 1.37 (control K diet) to 0.5 in the cortical collecting duct and increased the tyrosine phosphorylation of ROMK in the renal cortex and outer medulla. In contrast, the tempol treatment not only increased channel activity to 1.1 in the cortical collecting duct but also decreased the tyrosine phosphorylation of ROMK from rats on a KD diet. Finally, suppressing O(2)(-) production with tempol significantly increased renal K excretion measured with metabolic cage and lowered the plasma K concentration in comparison with those on a KD diet alone without tempol. We conclude that O(2)(-) and related products play a role in mediating the effect of low K intake on c-Src expression and in suppressing ROMK channel activity and renal K secretion.
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