ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2011
Hydrogen sulfide is a partially redox-independent activator of the human jejunum Na+ channel, Nav1.5.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- Role of hydrogen sulfide in health and disease.MedComm · 2024Review
- A Possible Role of Tetrodotoxin-Sensitive NaInternational journal of molecular sciences · 2024Article
- The Role of HAdvances in experimental medicine and biology · 2021Article
- Hydrogen sulfide, oxygen, and calcium regulation in developing human airway smooth muscle.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Inhibition of RhoA/Rho kinase pathway and smooth muscle contraction by hydrogen sulfide.Pharmacology research & perspectives · 2017Article
- Augmentation of cGMP/PKG pathway and colonic motility by hydrogen sulfide.American journal of physiology. Gastrointestinal and liver physiology · 2017Article
- Hydrogen sulphide as a signalling molecule regulating physiopathological processes in gastrointestinal motility.British journal of pharmacology · 2017Review
- Ranolazine inhibits voltage-gated mechanosensitive sodium channels in human colon circular smooth muscle cells.American journal of physiology. Gastrointestinal and liver physiology · 2015Article
- Actions of a hydrogen sulfide donor (NaHS) on transient sodium, persistent sodium, and voltage-gated calcium currents in neurons of the subfornical organ.Journal of neurophysiology · 2015Article
- Inhibition of RhoA-dependent pathway and contraction by endogenous hydrogen sulfide in rabbit gastric smooth muscle cells.American journal of physiology. Cell physiology · 2015Article
- The Cardioprotective Effects of Hydrogen Sulfide in Heart Diseases: From Molecular Mechanisms to Therapeutic Potential.Oxidative medicine and cellular longevity · 2015Review
- H2S and its role in redox signaling.Biochimica et biophysica acta · 2014Review
- Inhibition of the cardiac Na⁺ channel Nav1.5 by carbon monoxide.The Journal of biological chemistry · 2014Article
- Aggravation of seizure-like events by hydrogen sulfide: involvement of multiple targets that control neuronal excitability.CNS neuroscience & therapeutics · 2014Article
- Hydrogen sulfide signaling in the gastrointestinal tract.Antioxidants & redox signaling · 2014Review
- Release of GLP-1 and PYY in response to the activation of G protein-coupled bile acid receptor TGR5 is mediated by Epac/PLC-ε pathway and modulated by endogenous H2S.Frontiers in physiology · 2014Article
- Effects of hydrogen sulphide on motility patterns in the rat colon.British journal of pharmacology · 2013Article
- Hydrogen sulfide as an allosteric modulator of ATP-sensitive potassium channels in colonic inflammation.Molecular pharmacology · 2013Article
- Article
- Depolarizing actions of hydrogen sulfide on hypothalamic paraventricular nucleus neurons.PloS one · 2013Article
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Hydrogen sulfide (H(2)S) is produced endogenously by L-cysteine metabolism. H(2)S modulates several ion channels with an unclear mechanism of action. A possible mechanism is through reduction-oxidation reactions attributable to the redox potential of the sulfur moiety. The aims of this study were to determine the effects of the H(2)S donor NaHS on Na(V)1.5, a voltage-dependent sodium channel expressed in the gastrointestinal tract in human jejunum smooth muscle cells and interstitial cells of Cajal, and to elucidate whether H(2)S acts on Na(V)1.5 by redox reactions. Whole cell Na(+) currents were recorded in freshly dissociated human jejunum circular myocytes and Na(V)1.5-transfected human embryonic kidney-293 cells. RT-PCR amplified mRNA for H(2)S enzymes cystathionine β-synthase and cystathionine γ-lyase from the human jejunum. NaHS increased native Na(+) peak currents and shifted the half-point (V(1/2)) of steady-state activation and inactivation by +21 ± 2 mV and +15 ± 3 mV, respectively. Similar effects were seen on the heterologously expressed Na(V)1.5 α subunit with EC(50)s in the 10(-4) to 10(-3) M range. The reducing agent dithiothreitol (DTT) mimicked in part the effects of NaHS by increasing peak current and positively shifting steady-state activation. DTT together with NaHS had an additive effect on steady-state activation but not on peak current, suggesting that the latter may be altered via reduction. Pretreatment with the Hg(2+)-conjugated oxidizer thimerosal or the alkylating agent N-ethylmaleimide inhibited or decreased NaHS induction of Na(V)1.5 peak current. These studies show that H(2)S activates the gastrointestinal Na(+) channel, and the mechanism of action of H(2)S is partially redox independent.
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