Acetylcholine- and Sodium Hydrosulfide^|^ndash;Induced Endothelium-Dependent Relaxation and Hyperpolarization in Cerebral Vessels of Global Cerebral Ischemia^|^ndash;Reperfusion Rat

Han, Jun Hyun; Chen, Zhiwu; He, Guo‐Wei

doi:10.1254/jphs.12277fp

Cited by 29 publications

(26 citation statements)

References 41 publications

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“…H 2 S shares many features with NO. Accumulating evidence supports the concept that H 2 S acts as both EDRF and EDHF (Baragatti et al 2013;Han et al 2013;Skovgaard et al 2011;Wang 2009) (Fig. 2).…”

Section: H 2 S Acts As An Endothelium-derived Relaxing Factor (Edrf) supporting

confidence: 53%

H2S and Blood Vessels: An Overview

Yang

Wang

2015

Handbook of Experimental Pharmacology

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The physiological and biomedical importance of hydrogen sulfide (H2S) has been fully recognized in the cardiovascular system as well as in the rest of the body. In blood vessels, cystathionine γ-lyase (CSE) is a major H2S-producing enzyme expressed in both smooth muscle and endothelium as well as periadventitial adipose tissues. Regulation of H2S production from CSE is controlled by a complex integration of transcriptional, posttranscriptional, and posttranslational mechanisms in blood vessels. In smooth muscle cells, H2S regulates cell apoptosis, phenotypic switch, relaxation and contraction, and calcification. In endothelial cells, H2S controls cell proliferation, cellular senescence, oxidative stress, inflammation, etc. H2S interacts with nitric oxide and acts as an endothelium-derived relaxing factor and an endothelium-derived hyperpolarizing factor. H2S generated from periadventitial adipose tissues acts as an adipocyte-derived relaxing factor and modulates the vascular tone. Extensive evidence has demonstrated the beneficial roles of the CSE/H2S system in various blood vessel diseases, such as hypertension, atherosclerosis, and aortic aneurysm. The important roles signaling in the cardiovascular system merit further intensive and extensive investigation. H2S-releasing agents and CSE activators will find their great applications in the prevention and treatment of blood vessel-related disorders.

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Section: H 2 S Acts As An Endothelium-derived Relaxing Factor (Edrf) supporting

confidence: 53%

H2S and Blood Vessels: An Overview

Yang

Wang

2015

Handbook of Experimental Pharmacology

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“…These results indicate that there are EDHF-mediated responses in rat MCA. This is consistent with previous studies [27,33]. Furthermore, we have, for the first time, demonstrated that EDHF-mediated responses also exist in the rat CBA, the principal artery supplying the cerebellum, brain stem and other encephalic regions.…”

Section: Discussionsupporting

confidence: 93%

“…Our previous studies [26,27] also demonstrated that ACh-induced non-NO/PGI 2 -mediated hyperpolarization and dilation in rat cerebral arteries are abolished by the CSE inhibitor propargylglycine, and that the H 2 S donor NaHS (and L -cysteine, the substrate of endogenous H 2 S), elicited similar responses to ACh and was inhibited by 1 mmol/l TEA. High doses of TEA, a relatively nonspecific K + channel blocker, is not ‘specific' to K Ca channels, but, at low doses (≤5 mmol/l), it specifically inhibits K Ca channels in VSMC [26,30,31].…”

Section: Discussionmentioning

confidence: 84%

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Involvement of Hydrogen Sulfide in Endothelium-Derived Relaxing Factor-Mediated Responses in Rat Cerebral Arteries

Wang¹,

Hu²,

Fan

et al. 2016

J Vasc Res

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Background/Aim: H₂S is a novel vasoactivator. To verify the hypothesis that H₂S may act as an endothelium-derived hyperpolarizing factor (EDHF) in the rat cerebrovasculature, the role of H₂S in endothelium-derived relaxing factor (EDRF)-mediated responses was investigated. Methods: Cystathionine-γ-lyase (CSE) was knocked down with an siRNA technique. Artery diameter, hyperpolarization and Ca²⁺-activated K⁺ (K_Ca) current were measured. Results: CSE knockdown was indicated by a decrease in protein and mRNA expression in the rat middle cerebral artery (MCA) and cerebral basilar artery (CBA). Acetylcholine (ACh) induced significant hyperpolarization and vasodilation in endothelium-intact MCA and CBA. Removal of the endothelium abolished these responses. The nitric oxide (NO) synthase inhibitor L-NAME, but not the PGI₂ production inhibitor indomethacin, significantly inhibited ACh-induced hyperpolarization and vasodilation in the CBA. In the presence of L-NAME and indomethacin, ACh-induced hyperpolarization and vasodilation in the MCA and CBA were attenuated. The non-NO/PGI₂-mediated responses were abolished by the K_Ca channel blockers charybdotoxin and apamin. In the cerebral arteries from the CSE knockdown rat, non-NO/PGI₂-mediated responses were significantly attenuated, and the remaining responses were abolished by charybdotoxin and apamin or the CSE inhibitor propargylglycine. CSE knockdown did not affect L-NAME-sensitive responses in the CBA. Sodium hydrosulfide (NaHS) augmented the K_Ca current in CBA vascular smooth muscle cells. Conclusion: EDHF-mediated responses in rat cerebral arteries were due to H₂S activating the K_Ca channel.

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“…However, the chemical nature of EDHF in cerebral arteries is still unclear. Others [22] and we [23] have found that the endogenous gas hydrogen sulphide (H 2 S) is related to the action of EDHF in cerebral arteries.…”

Section: Introductionmentioning

confidence: 99%

Protective Effect and Mechanism of Total Flavones from Rhododendron simsii Planch on Endothelium‐Dependent Dilatation and Hyperpolarization in Cerebral Ischemia‐Reperfusion and Correlation to Hydrogen Sulphide Release in Rats

Han

Chen

2014

Evidence-Based Complementary and Alternative Medicine

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We for the first time investigated the effect and mechanism of the total flavones of Rhododendron simsii Planch (TFR), a widely-used Chinese herb for a thousand years, on vasodilatation and hyperpolarization in middle cerebral artery (MCA) of rats subject to global cerebral ischemia-reperfusion (CIR). TFR (11~2700 mg/L) evoked dose-dependent vasodilation and hyperpolarization in MCA of both sham and CIR that were partially inhibited by 30 μM N-nitro-L-arginine-methyl-ester and 10 μM indomethacin and further attenuated by endogenous H2S synthese-CSE inhibitor PPG (100 μM) or Ca2+-activated potassium channel (Kca) inhibitor TEA (1 mM). In whole-cell patch clamp recording, TFR remarkably enhanced the outward current that was inhibited by TEA. CIR increased CSE mRNA expression and the contents of H2S that were further increased by TFR. We conclude that, in MCA of CIR rats, TFR induces non-NO and non-PGI2-mediated effects of vasodilatation and hyperpolarization involving Kca and increases CSE mRNA expression level in endothelial cells and H2S content in the cerebrum. These findings suggest that the response induced by TFR is potentially related to endothelium-derived hyperpolarizing factor mediated by the endogenous H2S and promote the use of TFR in protection of brain from ischemia-reperfusion injury.

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Acetylcholine- and Sodium Hydrosulfide^|^ndash;Induced Endothelium-Dependent Relaxation and Hyperpolarization in Cerebral Vessels of Global Cerebral Ischemia^|^ndash;Reperfusion Rat

Cited by 29 publications

References 41 publications

H2S and Blood Vessels: An Overview

H2S and Blood Vessels: An Overview

Involvement of Hydrogen Sulfide in Endothelium-Derived Relaxing Factor-Mediated Responses in Rat Cerebral Arteries

Protective Effect and Mechanism of Total Flavones from Rhododendron simsii Planch on Endothelium‐Dependent Dilatation and Hyperpolarization in Cerebral Ischemia‐Reperfusion and Correlation to Hydrogen Sulphide Release in Rats

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