ArticleBritish journal of pharmacology2013
Hydrogen sulphide-mediated vasodilatation involves the release of neurotransmitters from sensory nerves in pressurized mesenteric small arteries isolated from rats.
Article in British journal of pharmacology, 2013. 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, 45 citations in OpenAlex.
- The Role of Hydrogen Sulfide in Peripheral Nervous System Modulation.Handbook of experimental pharmacology · 2026Review
- Homocysteine Attack on Vascular Endothelium-Old and New Features.International journal of molecular sciences · 2025Review
- Role of hydrogen sulfide in health and disease.MedComm · 2024Review
- Inhibitors of NLRP3 Inflammasome Formation: A Cardioprotective Role for the Gasotransmitters Carbon Monoxide, Nitric Oxide, and Hydrogen Sulphide in Acute Myocardial Infarction.International journal of molecular sciences · 2024Review
- Hydrogen Sulfide-Induced Vasodilation: The Involvement of Vascular Potassium Channels.Frontiers in pharmacology · 2022Review
- Vasorelaxation elicited by endogenous and exogenous hydrogen sulfide in mouse mesenteric arteries.Naunyn-Schmiedeberg's archives of pharmacology · 2020Article
- Hydrogen sulfide: a gaseous signaling molecule modulates tissue homeostasis: implications in ophthalmic diseases.Cell death & disease · 2019Review
- Effects of sulfide and polysulfides transmitted by direct or signal transduction-mediated activation of TRPA1 channels.British journal of pharmacology · 2019Review
- Role of Endothelial Dysfunction in Cardiovascular Diseases: The Link Between Inflammation and Hydrogen Sulfide.Frontiers in pharmacology · 2019Review
- Sulfur-containing gaseous signal molecules, ion channels and cardiovascular diseases.British journal of pharmacology · 2018Review
- Role of thiosulfate in hydrogen sulfide-dependent redox signaling in endothelial cells.American journal of physiology. Heart and circulatory physiology · 2017Article
- Capsaicin-Sensitive Sensory Nerves Mediate the Cellular and Microvascular Effects of H2S via TRPA1 Receptor Activation and Neuropeptide Release.Journal of molecular neuroscience : MN · 2016Article
- Chloride channels mediate sodium sulphide-induced relaxation in rat uteri.British journal of pharmacology · 2015Article
- Hydrogen sulfide and endothelium-dependent vasorelaxation.Molecules (Basel, Switzerland) · 2014Review
- Calcitonin gene-related peptide: physiology and pathophysiology.Physiological reviews · 2014Review
- The TRPA1 channel in migraine mechanism and treatment.British journal of pharmacology · 2014Review
- H2S relaxes isolated human airway smooth muscle cells via the sarcolemmal K(ATP) channel.Biochemical and biophysical research communications · 2014Article
- Article
- Modulation of hydrogen sulfide by vascular hypoxia.Hypoxia (Auckland, N.Z.) · 2014Review
- Transport of H2S and HS(-) across the human red blood cell membrane: rapid H2S diffusion and AE1-mediated Cl(-)/HS(-) exchange.American journal of physiology. Cell physiology · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
background and purposeHydrogen sulphide (H(2)S) is a gas that has recently been shown to have biological activity. In the majority of blood vessels studied so far, H(2)S has been shown to cause vasorelaxation, although contractile responses have been reported. In the present study, we have made a pharmacological assessment of the effects of H(2)S in mesenteric small arteries isolated from rats. EXPERIMENTAL APPROACH: Rat mesenteric small arteries were studied using pressure myography. In pressurised arteries, responses were obtained to the H(2)S donor, sodium hydrogen sulphide (NaHS), in the absence and presence of the NOS inhibitor L-NAME, raised extracellular potassium, the K(ATP) channel inhibitor glibenclamide, the Cl- channel blockers DIDS, NPPB and A9C, the TRPV1 receptor desensitizing agent, capsaicin, the CGRP antagonist, olcegepant, the TRPV1 channel blocker capsazepine and the TRPA1 channel blocker HC-030031. KEY
resultsNaHS produced a vasodilator response in rat mesenteric small arteries held at 90 mmHg. Responses to NaHS were not reproducible. Neither, glibenclamide nor, L-NAME inhibited responses to NaHS. DIDS abolished vasodilator responses to NaHS, but these were unaffected by the chloride channel blockers, NPPB and A9C. Responses to NaHS were attenuated after capsaicin pre-treatment, by a CGRP receptor antagonist and an inhibitor of TRPA1 channels. CONCLUSIONS AND IMPLICATIONS: In small arteries isolated from the rat mesentery, NaHS caused a vasodilatation. This response was not reproducible in vitro, since it was mediated by the release of sensory neurotransmitters in a capsaicin-like action. This release was mediated by a H(2)S-induced activation of TRPA1 channels.
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