ArticleNaunyn-Schmiedeberg's archives of pharmacology2012
An investigation of the mechanisms of hydrogen sulfide-induced vasorelaxation in rat middle cerebral arteries.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2012. 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, 42 citations in OpenAlex.
- Complex Pathophysiology of Acute Kidney Injury (AKI) in Aging: Epigenetic Regulation, Matrix Remodeling, and the Healing Effects of HBiomolecules · 2024Review
- Chemistry of Hydrogen Sulfide-Pathological and Physiological Functions in Mammalian Cells.Cells · 2023Review
- Review
- Roles of the RhoA-ROCK Signaling Pathway in the Endothelial HACS omega · 2022Article
- Hydrogen Sulfide-Induced Vasodilation: The Involvement of Vascular Potassium Channels.Frontiers in pharmacology · 2022Review
- GYY4137 and Sodium Hydrogen Sulfide Relaxations Are Inhibited by L-Cysteine and KFrontiers in pharmacology · 2021Article
- The Potential Role of Hydrogen Sulfide in the Regulation of Cerebrovascular Tone.Biomolecules · 2020Review
- Vasorelaxation elicited by endogenous and exogenous hydrogen sulfide in mouse mesenteric arteries.Naunyn-Schmiedeberg's archives of pharmacology · 2020Article
- Article
- TRPP2 associates with STIM1 to regulate cerebral vasoconstriction and enhance high salt intake-induced hypertensive cerebrovascular spasm.Hypertension research : official journal of the Japanese Society of Hypertension · 2019Article
- Emerging role of hydrogen sulfide in hypertension and related cardiovascular diseases.British journal of pharmacology · 2015Review
- Hydrogen Sulfide Targets the Cys320/Cys529 Motif in Kv4.2 to Inhibit the Ito Potassium Channels in Cardiomyocytes and Regularizes Fatal Arrhythmia in Myocardial Infarction.Antioxidants & redox signaling · 2015Article
- Chloride channels mediate sodium sulphide-induced relaxation in rat uteri.British journal of pharmacology · 2015Article
- Hydrogen sulfide treatment reduces blood pressure and oxidative stress in angiotensin II-induced hypertensive mice.Hypertension research : official journal of the Japanese Society of Hypertension · 2015Article
- H2S relaxes isolated human airway smooth muscle cells via the sarcolemmal K(ATP) channel.Biochemical and biophysical research communications · 2014Article
- Contribution of hydrogen sulfide to the control of coronary blood flow.Microcirculation (New York, N.Y. : 1994) · 2014Article
- Modulation of hydrogen sulfide by vascular hypoxia.Hypoxia (Auckland, N.Z.) · 2014Review
- Hydrogen sulfide protects endothelial nitric oxide function under conditions of acute oxidative stress in vitro.Naunyn-Schmiedeberg's archives of pharmacology · 2014Article
- Effect of type 1 diabetes on the production and vasoactivity of hydrogen sulfide in rat middle cerebral arteries.Physiological reports · 2013Article
- Hydrogen sulfide as a vasculoprotective factor.Medical gas research · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hydrogen sulfide (H(2)S) is an endogenous mediator with peripheral vasorelaxant effects; however, the mechanism of H(2)S-induced vasorelaxation in cerebral blood vessels has not been extensively studied. Vasorelaxation studies were performed on middle cerebral arteries from male Sprague Dawley rats using wire myography. Immunofluorescence staining was used to detect the presence of the H(2)S-producing enzyme cystathionine-γ-lyase (CSE). CSE was present in the endothelium and smooth muscle of middle cerebral arteries. The CSE substrate, L-cysteine, induced vasorelaxation that was sensitive to the CSE inhibitor DL-propargylglycine. This relaxation was independent of endothelium, suggesting that H(2)S was produced in the vascular smooth muscle. The H(2)S donor, sodium hydrogen sulfide (NaHS; 0.1-3.0 mM) produced concentration-dependent relaxation, which was unaffected by endothelium removal. Nifedipine (3 μM) significantly reduced the maximum relaxation elicited by NaHS. Inhibiting potassium (K(+)) conductance with 50 mM K(+) significantly attenuated NaHS-induced relaxation, however, selective blockers of ATP sensitive (K(ATP)), calcium sensitive (K(Ca)), voltage dependent (K(V)), or inward rectifier (K(ir)) channels alone or in combination did not affect the response to NaHS. 4,4-diisothiocyanatostilbene-2,2-disulfonic acid (DIDS; 300 μM) caused a significant rightward shift of the NaHS concentration-response curve, but this effect could not be explained by inhibition of Cl(-) channels or Cl(-)/HCO (3)(-) exchange, as selective blockade of these mechanisms had no effect. These findings suggest endogenous H(2)S can regulate cerebral vascular function. The H(2)S-mediated relaxation of middle cerebral arteries is DIDS sensitive and partly mediated by inhibition of L-type calcium channels, with an additional contribution by K channels but not K(ATP), K(Ca), K(V), or K(ir) subtypes.
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