ArticleHypertension (Dallas, Tex. : 1979)2014
Protein kinase G Iα oxidation paradoxically underlies blood pressure lowering by the reductant hydrogen sulfide.
Article in Hypertension (Dallas, Tex. : 1979), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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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
56 citing papers in PubMed, 101 citations in OpenAlex.
- Hydropersulfides promote angiogenesis and preserve vascular function.Redox biology · 2026Article
- A redox sensor in protein kinase A regulatory subunit Iα regulates vasodilation and protects against hypertension.Redox biology · 2026Article
- Physiological Roles of Hydrogen Sulfide/Polysulfides and Regulation of their Production.Handbook of experimental pharmacology · 2026Review
- Hydrogen sulfide/polysulfides signaling and neuronal diseases.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Reactive Sulfur Species and Protein Persulfidation: An Emerging Redox Axis in Human Health and Disease.Current issues in molecular biology · 2025Review
- The Role of Hydrogen Sulfide in the Regulation of the Pulmonary Vasculature in Health and Disease.Antioxidants (Basel, Switzerland) · 2025Review
- Hydrogen Sulfide (HBiomolecules · 2024Review
- Health position paper and redox perspectives on reactive oxygen species as signals and targets of cardioprotection.Redox biology · 2023Review
- SOD1 is an essential HProceedings of the National Academy of Sciences of the United States of America · 2023Article
- The role of sulfur compounds in chronic obstructive pulmonary disease.Frontiers in molecular biosciences · 2022Review
- Endogenous Hemoprotein-Dependent Signaling Pathways of Nitric Oxide and Nitrite.Inorganic chemistry · 2021Review
- Methods in sulfide and persulfide research.Nitric oxide : biology and chemistry · 2021Article
- Hydrogen Sulfide (HBiomolecules · 2021Review
- Endothelium as a Source and Target of HAntioxidants (Basel, Switzerland) · 2021Review
- Cardiovascular "Patterns" of HBiomolecules · 2021Article
- Hydrogen sulfide and vascular regulation - An update.Journal of advanced research · 2021Review
- Role of Hydrogen Sulfide and Polysulfides in Neurological Diseases: Focus on Protein S-Persulfidation.Current neuropharmacology · 2021Review
- Hydrogen Sulfide and Carnosine: Modulation of Oxidative Stress and Inflammation in Kidney and Brain Axis.Antioxidants (Basel, Switzerland) · 2020Review
- Hydrogen sulfide signalling in the CNS - Comparison with NO.British journal of pharmacology · 2020Review
- Estrogen Receptors and Estrogen-Induced Uterine Vasodilation in Pregnancy.International journal of molecular sciences · 2020Review
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Abstract
Dysregulated blood pressure control leading to hypertension is prevalent and is a risk factor for several common diseases. Fully understanding blood pressure regulation offers the possibility of developing rationale therapies to alleviate hypertension and associated disease risks. Although hydrogen sulfide (H2S) is a well-established endogenous vasodilator, the molecular basis of its blood-pressure lowering action is incompletely understood. H2S-dependent vasodilation and blood pressure lowering in vivo was mediated by it catalyzing formation of an activating interprotein disulfide within protein kinase G (PKG) Iα. However, this oxidative activation of PKG Iα is counterintuitive because H2S is a thiol-reducing molecule that breaks disulfides, and so it is not generally anticipated to induce their formation. This apparent paradox was explained by H2S in the presence of molecular oxygen or hydrogen peroxide rapidly converting to polysulfides, which have oxidant properties that in turn activate PKG by inducing the disulfide. These observations are relevant in vivo because transgenic knockin mice in which the cysteine 42 redox sensor within PKG has been systemically replaced with a redox-dead serine residue are resistant to H2S-induced blood pressure lowering. Thus, a primary mechanism by which the reductant molecule H2S lowers blood pressure is mediated somewhat paradoxically by the oxidative activation of PKG.
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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.