ArticlePflugers Archiv : European journal of physiology2015
Hydrogen peroxide induces vasorelaxation by enhancing 4-aminopyridine-sensitive Kv currents through S-glutathionylation.
Article in Pflugers Archiv : European journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 56 citations in OpenAlex.
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- HBasic research in cardiology · 2025Article
- HInternational journal of molecular sciences · 2025Article
- Redox Regulation of KAntioxidants & redox signaling · 2024Review
- Basal NAD(H) redox state permits hydrogen peroxide-induced mesenteric artery dilatation.The Journal of physiology · 2023Article
- Review
- The role of glutathione peroxidase-1 in health and disease.Free radical biology & medicine · 2022Review
- Article
- Modulation of Renal Function in a Metabolic Syndrome Rat Model by Antioxidants inMolecules (Basel, Switzerland) · 2021Article
- NO-induced vasodilation correlates directly with BP in smooth muscle-Na/Ca exchanger-1-engineered mice: elevated BP does not attenuate endothelial function.American journal of physiology. Heart and circulatory physiology · 2021Article
- S-glutathionylation, friend or foe in cardiovascular health and disease.Redox biology · 2020Review
- Metabolic regulation of endothelial SK channels and human coronary microvascular function.International journal of cardiology · 2020Article
- Vasodilation of Tea Polyphenols Ex Vivo Is Mediated by Hydrogen Peroxide Under Rapid Compound Decay.Antioxidants (Basel, Switzerland) · 2020Article
- In vitro effects of hydrogen peroxide on rat uterine contraction before and during pregnancy.Croatian medical journal · 2018Article
- Superoxide via Sp3 mechanism increases renal renin activity, renal AT1 receptor function, and blood pressure in rats.American journal of physiology. Renal physiology · 2018Article
- Coronary microvascular Kv1 channels as regulatory sensors of intracellular pyridine nucleotide redox potential.Microcirculation (New York, N.Y. : 1994) · 2018Review
- Shaker-related voltage-gated KMicrocirculation (New York, N.Y. : 1994) · 2018Article
- KMicrocirculation (New York, N.Y. : 1994) · 2018Review
- KMicrocirculation (New York, N.Y. : 1994) · 2018Review
- Caveolar remodeling is a critical mechanotransduction mechanism of the stretch-induced L-type CaPflugers Archiv : European journal of physiology · 2017Article
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10 authors at 4 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Hydrogen peroxide (H2O2) is an endothelium-derived hyperpolarizing factor. Since opposing vasoactive effects have been reported for H2O2 depending on the vascular bed and experimental conditions, this study was performed to assess whether H2O2 acts as a vasodilator in the rat mesenteric artery and, if so, to determine the underlying mechanisms. H2O2 elicited concentration-dependent relaxation in mesenteric arteries precontracted with norepinephrine. The vasodilatory effect of H2O2 was reversed by treatment with dithiothreitol. H2O2-elicited vasodilation was significantly reduced by blocking 4-aminopyridine (4-AP)-sensitive Kv channels, but it was resistant to blockers of big-conductance Ca(2+)-activated K(+) channels and inward rectifier K(+) channels. A patch-clamp study in mesenteric arterial smooth muscle cells (MASMCs) showed that H2O2 increased Kv currents in a concentration-dependent manner. H2O2 speeded up Kv channel activation and shifted steady state activation to hyperpolarizing potentials. Similar channel activation was seen with oxidized glutathione (GSSG). The H2O2-mediated channel activation was prevented by glutathione reductase. Consistent with S-glutathionylation, streptavidin pull-down assays with biotinylated glutathione ethyl ester showed incorporation of glutathione (GSH) in the Kv channel proteins in the presence of H2O2. Interestingly, conditions of increased oxidative stress within MASMCs impaired the capacity of H2O2 to stimulate Kv channels. Not only was the H2O2 stimulatory effect much weaker, but the inhibitory effect of H2O2 was unmasked. These data suggest that H2O2 activates 4-AP-sensitive Kv channels, possibly through S-glutathionylation, which elicits smooth muscle relaxation in rat mesenteric arteries. Furthermore, our results support the idea that the basal redox status of MASMCs determines the response of Kv currents to H2O2.
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