ArticleOxidative medicine and cellular longevity2015
Superoxide Mediates Depressive Effects Induced by Hydrogen Sulfide in Rostral Ventrolateral Medulla of Spontaneously Hypertensive Rats.
Article in Oxidative medicine and cellular longevity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 17 citations in OpenAlex.
- Beneficial Effects of Putative Hydrogen Sulfide (HMolecules (Basel, Switzerland) · 2026Article
- Mechanism of paraventricular nucleus HPhysiological reports · 2026Article
- Hydrogen sulfide production in the medullary respiratory center modulates the neural circuit for respiratory pattern and rhythm generations.Scientific reports · 2023Article
- Targeting hydrogen sulfide and nitric oxide to repair cardiovascular injury after trauma.Nitric oxide : biology and chemistry · 2022Review
- The Inhibitory Role of Hydrogen Sulfide in UII-Induced Cardiovascular Effects and the Underlying Signaling Pathways.Antioxidants (Basel, Switzerland) · 2022Article
- Central Administration of Hydrogen Sulfide Donor NaHS Reduces Iba1-Positive Cells in the PVN and Attenuates Rodent Angiotensin II Hypertension.Frontiers in neuroscience · 2021Article
- Gut microbiota and neuroinflammation in pathogenesis of hypertension: A potential role for hydrogen sulfide.Pharmacological research · 2020Review
- CBS-Induced HEvidence-based complementary and alternative medicine : eCAM · 2020Article
- Gasotransmitter Heterocellular Signaling.Antioxidants & redox signaling · 2017Article
- Hydrogen Sulfide Regulates the [CaOxidative medicine and cellular longevity · 2016Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hydrogen sulfide (H2S) plays a crucial role in the regulation of blood pressure and oxidative stress. In the present study, we tested the hypothesis that H2S exerts its cardiovascular effects by reducing oxidative stress via inhibition of NADPH oxidase activity in the rostral ventrolateral medulla (RVLM). We examined cell distributions of cystathionine-β-synthase (CBS) and effects of H2S on reactive oxygen species (ROS) and mean arterial blood pressure (MAP) in spontaneously hypertensive rats (SHRs). We found that CBS was expressed in neurons of the RVLM, and the expression was lower in SHRs than in Wistar-Kyoto rats. Microinjection of NaHS (H2S donor), S-adenosyl-l-methionine (SAM, a CBS agonist), or Apocynin (NADPH oxidase inhibitor) into the RVLM reduced the ROS level, NADPH oxidase activity, and MAP, whereas microinjection of hydroxylamine hydrochloride (HA, a CBS inhibitor) increased MAP. Furthermore, intracerebroventricular infusion of NaHS inhibited phosphorylation of p47(phox), a key step of NADPH oxidase activation. Since decreasing ROS level in the RVLM reduces MAP and heart rate and increasing H2S reduces ROS production, we conclude that H2S exerts an antihypertensive effect via suppressing ROS production. H2S, as an antioxidant, may be a potential target for cardiovascular diseases.
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