ArticleAmerican journal of physiology. Heart and circulatory physiology2013
Hydrogen sulfide dilates rat mesenteric arteries by activating endothelial large-conductance Ca²⁺-activated K⁺ channels and smooth muscle Ca²⁺ sparks.
Article in American journal of physiology. Heart and circulatory physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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66 citing papers in PubMed, 113 citations in OpenAlex.
- Guidelines for evaluating endothelial function in vascular tissue.American journal of physiology. Heart and circulatory physiology · 2026Review
- Black gas, bright future: HNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Redox Regulation of Endogenous Gasotransmitters in Vascular Health and Disease.International journal of molecular sciences · 2025Review
- Clinical Applications for Gasotransmitters in the Cardiovascular System: Are We There Yet?International journal of molecular sciences · 2023Review
- A novel, microvascular evaluation method and device for early diagnosis of peripheral artery disease and chronic limb-threatening ischemia in individuals with diabetes.Journal of vascular surgery cases and innovative techniques · 2023Article
- CaInternational journal of molecular sciences · 2023Review
- Reactive Oxygen Species-Triggered Hydrogen Sulfide Release and Cancer-Selective Antiproliferative Effect of Anethole Dithiolethione-Containing Polymeric Micelles.Advanced healthcare materials · 2023Article
- Region-Specific and Pregnancy-Enhanced Vasodilator Effects of Hydrogen Sulfide.Obstetrics and gynecology research · 2023Article
- Targeting hydrogen sulfide and nitric oxide to repair cardiovascular injury after trauma.Nitric oxide : biology and chemistry · 2022Review
- Role of Cholesterol in the Regulation of Hydrogen Sulfide Signaling within the Vascular Endothelium.Antioxidants (Basel, Switzerland) · 2022Article
- Vasoactive Effects of Chronic Treatment with Fructose and Slow-Releasing HInternational journal of molecular sciences · 2022Article
- Vasorelaxant Activity of AP39, a Mitochondria-Targeted HBiomolecules · 2022Article
- Hydrogen Sulfide-Induced Vasodilation: The Involvement of Vascular Potassium Channels.Frontiers in pharmacology · 2022Review
- Clinical Use of Hydrogen Sulfide to Protect Against Intimal Hyperplasia.Frontiers in cardiovascular medicine · 2022Review
- A Case for Hydrogen Sulfide Metabolism as an Oxygen Sensing Mechanism.Antioxidants (Basel, Switzerland) · 2021Review
- Hydrogen Sulfide Actions in the Vasculature.Comprehensive Physiology · 2021Article
- The vasodilatory mechanism of nitric oxide and hydrogen sulfide in the human mesenteric artery in patients with colorectal cancer.Experimental and therapeutic medicine · 2021Article
- Simulated sleep apnea alters hydrogen sulfide regulation of blood flow and pressure.American journal of physiology. Heart and circulatory physiology · 2021Article
- Interaction among Hydrogen Sulfide and Other Gasotransmitters in Mammalian Physiology and Pathophysiology.Advances in experimental medicine and biology · 2021Review
- GYY4137 and Sodium Hydrogen Sulfide Relaxations Are Inhibited by L-Cysteine and KFrontiers in pharmacology · 2021Article
6 more citing papers are in PubMed but not listed here.
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7 authors at 1 institution in 1 country.
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Abstract
We have previously shown that hydrogen sulfide (H₂S) reduces myogenic tone and causes relaxation of phenylephrine (PE)-constricted mesenteric arteries. This effect of H₂S to cause vasodilation and vascular smooth muscle cell (VSMC) hyperpolarization was mediated by large-conductance Ca(2+)-activated potassium channels (BKCa). Ca(2+) sparks are ryanodine receptor (RyR)-mediated Ca(2+)-release events that activate BKCa channels in VSMCs to cause membrane hyperpolarization and vasodilation. We hypothesized that H₂S activates Ca(2+) sparks in small mesenteric arteries. Ca(2+) sparks were measured using confocal microscopy in rat mesenteric arteries loaded with the Ca(2+) indicator fluo-4. VSMC membrane potential (Em) was measured in isolated arteries using sharp microelectrodes. In PE-constricted arteries, the H₂S donor NaHS caused vasodilation that was inhibited by ryanodine (RyR blocker), abluminal or luminal iberiotoxin (IbTx, BKCa blocker), endothelial cell (EC) disruption, and sulfaphenazole [cytochrome P-450 2C (Cyp2C) inhibitor]. The H₂S donor NaHS (10 μmol/l) increased Ca(2+) sparks but only in the presence of intact EC and this was blocked by sulfaphenazole or luminal IbTx. Inhibiting cystathionine γ-lyase (CSE)-derived H2S with β-cyano-l-alanine (BCA) also reduced VSMC Ca(2+) spark frequency in mesenteric arteries, as did EC disruption. However, excess CSE substrate homocysteine did not affect spark activity. NaHS hyperpolarized VSMC Em in PE-depolarized mesenteric arteries with intact EC and also hyperpolarized EC Em in arteries cut open to expose the lumen. This hyperpolarization was prevented by ryanodine, sulfaphenazole, and abluminal or luminal IbTx. BCA reduced IbTx-sensitive K(+) currents in freshly dispersed mesenteric ECs. These results suggest that H₂S increases Ca(2+) spark activity in mesenteric artery VSMC through activation of endothelial BKCa channels and Cyp2C, a novel vasodilatory pathway for this emerging signaling molecule.
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