ArticleCirculation research2011
Hydrogen sulfide as endothelium-derived hyperpolarizing factor sulfhydrates potassium channels.
Article in Circulation research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 298 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
298 citing papers in PubMed, 1 synthesis or guideline pooled it, 612 citations in OpenAlex.
- On the mechanisms of brain blood flow regulation during hypoxia.The Journal of physiology · 2025Pooled it
- Hydrogen sulfide-releasing hydrogels: a new perspective on clinical translation.Medical gas research · 2027Review
- Molecular Mechanisms Governing Vascular Function in Heart Failure.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Mechanisms Underlying the Biphasic Effects of Hydrogen Sulfide in Rat Intrapulmonary Arteries.Biomedicines · 2026Article
- Immunoresponsive Gene 1-Itaconate Exacerbates Hypertension by Inhibiting the Cystathionine Gamma-Lyase/Hydrogen Sulfide Pathway.Journal of cardiovascular development and disease · 2026Article
- Intracellular Crosstalk of the Gasotransmitter Trio (NO, CO, HInternational journal of molecular sciences · 2026Review
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- Hydrogen sulfide-mediated protein s-persulfidation: a regulatory mechanism in cardiovascular homeostasis.Molecular medicine (Cambridge, Mass.) · 2026Review
- The Role of Ferroptosis in Diabetes Pathogenesis: Therapeutic Implications of Hydrogen Sulfide and Its Reactive Metabolites.Antioxidants (Basel, Switzerland) · 2026Review
- S-sulfhydration: Novel insights into the antioxidant and antiinflammation in age-related diseases.Journal of advanced research · 2026Review
- The Chronic Elevated Consumption ofInternational journal of molecular sciences · 2026Article
- Naturally Occurring HHandbook of experimental pharmacology · 2026Review
- Hydrogen Sulfide Signaling in Neurodegenerative Movement Disorders.Handbook of experimental pharmacology · 2026Review
- Dietary methionine depletion and hydrogen sulfide-producing genes in perivascular adipose tissue of male Wistar rats.Physiological reports · 2025Article
- Black gas, bright future: HNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Exercise Enhances Anti-contractile Effects of PVAT Through Endogenous HCardiovascular drugs and therapy · 2025Article
- Hydrogen sulfide/polysulfides signaling and neuronal diseases.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Hydrogen sulfide in placental development and pregnancy disorders: mechanisms, therapeutic potential, and translational challenges.Reproductive biology and endocrinology : RB&E · 2025Review
- Hydrogen Sulfide Protects Erectile Function Through Stimulation of Antioxidant Defense in the Corpus Cavernosum: Insights From SG1002 Administration and Cystathionine γ-Lyase Knockout.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Detection of Protein Polysulfidation Using a β-(4-Hydroxyphenyl)ethyl Iodoacetamide-Derived Biotin Tag HPB.Analytical chemistry · 2025Article
238 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
rationaleNitric oxide, the classic endothelium-derived relaxing factor (EDRF), acts through cyclic GMP and calcium without notably affecting membrane potential. A major component of EDRF activity derives from hyperpolarization and is termed endothelium-derived hyperpolarizing factor (EDHF). Hydrogen sulfide (H(2)S) is a prominent EDRF, since mice lacking its biosynthetic enzyme, cystathionine γ-lyase (CSE), display pronounced hypertension with deficient vasorelaxant responses to acetylcholine.
objectiveThe purpose of this study was to determine if H(2)S is a major physiological EDHF. METHODS AND
resultsWe now show that H(2)S is a major EDHF because in blood vessels of CSE-deleted mice, hyperpolarization is virtually abolished. H(2)S acts by covalently modifying (sulfhydrating) the ATP-sensitive potassium channel, as mutating the site of sulfhydration prevents H(2)S-elicited hyperpolarization. The endothelial intermediate conductance (IK(Ca)) and small conductance (SK(Ca)) potassium channels mediate in part the effects of H(2)S, as selective IK(Ca) and SK(Ca) channel inhibitors, charybdotoxin and apamin, inhibit glibenclamide-insensitive, H(2)S-induced vasorelaxation.
conclusionsH(2)S is a major EDHF that causes vascular endothelial and smooth muscle cell hyperpolarization and vasorelaxation by activating the ATP-sensitive, intermediate conductance and small conductance potassium channels through cysteine S-sulfhydration. Because EDHF activity is a principal determinant of vasorelaxation in numerous vascular beds, drugs influencing H(2)S biosynthesis offer therapeutic potential.
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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.