H<sub>2</sub>S contributes to the hepatic arterial buffer response and mediates vasorelaxation of the hepatic artery via activation of K<sub>ATP</sub> channels

Siebert, Nikolai; Cantré, Daniel; Eipel, Christian; Vollmar, Brigitte

doi:10.1152/ajpgi.90484.2008

Cited by 64 publications

(47 citation statements)

References 33 publications

(53 reference statements)

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“…However, there were no significant differences after Glib treatment in the HF rats that were not treated with H-Are, which confirmed that the arecoline-mediated improvement in ACh-induced EDVR may be partly due to H 2 S-induced K ATP channel opening in VSMCs. Our findings were consistent with the results of Zhao et al [18,19] . This study demonstrated that H 2 S is different from NO and CO 2 and that H 2 S-induced vascular relaxation was mediated mainly by K ATP channel opening in VSMCs.…”

Section: Discussionsupporting

confidence: 94%

“…However, because of the experimental limitations, endogenous H 2 S levels in the thoracic aortas were not determined. Some studies also showed that H 2 S is the only endogenous gaseous K ATP channel opener and that H 2 S activated K ATP channels at the whole-cell and single channel levels in VSMCs [16,18,19] . Opening of K ATP channels leads to membrane hyperpolarization and relaxation of VSMCs.…”

Section: Discussionmentioning

confidence: 99%

“…Zhao et al reported that H 2 S relaxed rat aortic tissues in vitro in a K ATP channel-dependent manner [18] . Siebert et al showed that H 2 S mediated vasorelaxation of the hepatic artery by activation of K ATP channels [19] . Goto et al reported that areca seed extract led to endothelium-dependent vasodilation in rat aortas [20] .…”

Section: Introductionmentioning

confidence: 99%

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Arecoline improves vascular endothelial function in high fructose-fed rats via increasing cystathionine-γ-lyase expression and activating KATP channels

et al. 2012

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Aim:To investigate the effect of arecoline, a major component of betel nut, on vascular endothelial function in high fructose-fed rats and the potential mechanisms underlying the effect. Methods: Male Wistar rats were fed a high-fructose or control diet for 16 weeks. At the beginning of week 13, the rats were injected ip with low (0.5 mg·kg -1 ·d -1 ), medium (1.0 mg·kg -1 ·d -1 ) or high (5.0 mg·kg -1 ·d -1 ) doses of arecoline for 4 weeks. At the termination of the treatments, blood was collected, fasting blood glucose (FBG) and serum insulin (FSI) levels were measured, and insulin sensitivity index (ISI) was calculated. The thoracic aortas were isolated and aortic rings were prepared for studying ACh-induced endothelium-dependent vasorelaxation (EDVR). The mRNA and protein expression of cystathionine-γ-lyase (CSE) in the thoracic aortas was analyzed using RT-PCR and Western blot analysis, respectively. Results: In high fructose-fed rats, the levels of FBG and FSI were remarkably increased, whereas the ISI and the mRNA and protein expression of CSE were significantly decreased. ACh-induced EDVR in the aortic rings from high fructose-fed rats was remarkably reduced. These changes were reversed by treatment with high dose arecoline. Pretreatment of the aortic rings rings from high fructose-fed rats with the CSE inhibitor propargylglycine (10 mmol/L) or the ATP-sensitive potassium (K ATP ) channel blocker glibenclamide (10 mmol/L) abolished the restoration of ACh-induced EDVR by high dose arecoline. On the contrary, treatment with high dose arecoline significantly impaired ACh-induced EDVR in the aortic rings from control rats, and pretreatment with propargylglycine or glibenclamide did not cause further changes. Conclusion: Arecoline treatment improves ACh-induced EDVR in high fructose-fed rats, and the potential mechanism of action might be associated with increase of CSE expression and activation of K ATP channels by arecoline.

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Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 99%

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Arecoline improves vascular endothelial function in high fructose-fed rats via increasing cystathionine-γ-lyase expression and activating KATP channels

et al. 2012

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“…21 H 2 S can regulate vascular tone through several mechanisms, such as acting on ATP-sensitive potassium channels. [22][23][24] A recent study has found that H 2 S also affects transient receptor potential channels (TRPCs) in mesenchymal stem cells and regulates calcium homeostasis. 4 Our previous studies have demonstrated that TRPC3-mediated calcium signaling contributes to the development of hypertension, 25,26 but it is unclear whether the hypotensive effects of taurine and H 2 S are associated with modulation of TRPC3 channels in the vasculature.…”

mentioning

confidence: 99%

Taurine Supplementation Lowers Blood Pressure and Improves Vascular Function in Prehypertension

et al. 2016

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P rehypertension is highly prevalent worldwide.1 It is estimated that ≈30% to 50% of the population have this condition. It frequently complicates other cardiometabolic risk factors and is closely associated with coronary heart disease, stroke, and renal dysfunction.2 Early intervention in prehypertension substantially prevents the incidence of hypertension and related damage to target organs. Currently, several strategies are used to treat prehypertension, including the incorporation of therapeutic lifestyle changes, such as healthy dietary intake and regular physical activity, as well as the use of antihypertensive drugs, such as an angiotensin II receptor blocker. Although these treatments improve prehypertension, poor compliance and limitations associated with antihypertensive medications prevent their application in the general population. Thus, there is an urgent need to identify reliable and accurate measures to prevent the development of prehypertension.Taurine (2-aminoethanesulfonic acid) is the most abundant, semiessential, sulfur-containing amino acid. It can be synthesized in vivo by cysteine in the presence of cysteine dioxygenase, 3 but taurine is mainly acquired from dietary sources, such as eggs, meat, and seafood. Hydrogen sulfide (H 2 S) is synthesized from 2 sulfur-containing amino acids, l-cysteine and l-methionine, by the 3 enzymes, cystathionine-γ-lyase (CSE), cystathionine-β-synthetase (CBS), and 3-mercaptopyruvate sulfurtransferase. 4 Taurine has several potentially beneficial cardiovascular effects that involve regulation of the nitric oxide system and endothelial function, 5,6 the renin-angiotensin-aldosteroneAbstract-Taurine, the most abundant, semiessential, sulfur-containing amino acid, is well known to lower blood pressure (BP) in hypertensive animal models. However, no rigorous clinical trial has validated whether this beneficial effect of taurine occurs in human hypertension or prehypertension, a key stage in the development of hypertension. In this randomized, double-blind, placebo-controlled study, we assessed the effects of taurine intervention on BP and vascular function in prehypertension. We randomly assigned 120 eligible prehypertensive individuals to receive either taurine supplementation (1.6 g per day) or a placebo for 12 weeks. Taurine supplementation significantly decreased the clinic and 24-hour ambulatory BPs, especially in those with high-normal BP. Mean clinic systolic BP reduction for taurine/placebo was 7.2/2.6 mm Hg, and diastolic BP was 4.7/1.3 mm Hg. Mean ambulatory systolic BP reduction for taurine/placebo was 3.8/0.3 mm Hg, and diastolic BP was 3.5/0.6 mm Hg. In addition, taurine supplementation significantly improved endothelium-dependent and endothelium-independent vasodilation and increased plasma H 2 S and taurine concentrations. Furthermore, changes in BP were negatively correlated with both the plasma H 2 S and taurine levels in taurine-treated prehypertensive individuals. To further elucidate the hypotensive mechanism, experimental studies were perfor...

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“…The vasorelaxing action of NaHS, administrated at concentrations ranging from 50 µM to 100 µM, has been observed in rat aorta and hepatic artery [96,97], as well as in resistance mesenteric arteries [21], gastric artery and gastric mucosal circulation [98], cerebral arterioles and artery [99,100], pulmonary artery [101], and coronary artery [102]. Since NaHS is five-to-nine fold more potent in relaxing mesenteric arteries than thoracic aorta and pulmonary artery (EC 50 25 µM vs. 125 µM and 233 µM, respectively), it has been proposed as a key regulator of peripheral resistance arteries and, therefore, of blood pressure [15].…”

Section: The Roles Of H 2 S and No In Vasodilationmentioning

confidence: 99%

Hydrogen Sulfide and Endothelial Dysfunction: Relationship with Nitric Oxide

Altaany¹,

Moccia²,

Munaron³

et al. 2014

CMC

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The endothelium is a cellular monolayer that lines the inner surface of blood vessels and plays a central role in the maintenance of cardiovascular homeostasis by controlling platelet aggregation, vascular tone, blood fluidity and fibrinolysis, adhesion and transmigration of inflammatory cells, and angiogenesis. Endothelial dysfunctions are associated with various cardiovascular diseases, including atherosclerosis, hypertension, myocardial infarction, and cardiovascular complications of diabetes. Numerous studies have established the antiinflammatory, anti-apoptotic, and anti-oxidant effects of hydrogen sulfide (H 2 S), the latest member to join the gasotransmitter family along with nitric oxide and carbon monoxide, on vascular endothelium. In addition, H 2 S may prime endothelial cells (ECs) toward angiogenesis and contribute to wound healing, aside to its well-known ability to relax vascular smooth muscle cells (VSMCs), thereby reducing blood pressure. Finally, H 2 S may inhibit VSMC proliferation and platelet aggregation. Consistently, a deficit in H 2 S homeostasis is involved in the pathogenesis of atherosclerosis and of hyperglycaemic endothelial injury. Therefore, the application of H 2 S-releasing drugs or using gene therapy to increase endogenous H 2 S level may help restore endothelial function and antagonize the progression of cardiovascular diseases. The present article reviews recent studies on the role of H 2 S in endothelial homeostasis, under both physiological and pathological conditions, and its putative therapeutic applications. Endothelial structure and functionThe endothelium lines the luminal surface of the entire vascular tree and the cardiac chambers, where it is termed endocardium. As a consequence, the endothelium presents a rather broad extension (300 to 1000 m 2 ) and weight (1.5 kg), achieving sizes comparable to other vital organs of the human body [1,2]. The endothelium can, therefore, be regarded as a real "organ spread across the organism" [3] and, as such, not only it is important for the regulation of local tissue functions, but also for maintaining the whole organism homeostasis [4]. Vascular endothelial cells (ECs) possess a polarized architecture: their luminal membrane is directly exposed to hematic constituents and circulating cells, while the basolateral surface is separated from surrounding tissues by a glycoprotein basement membrane -the sub-endothelial basement -which is formed by fibronectin, laminin, and collagen and is secreted by ECs themselves [2].Heterogeneity is, however, the hallmark of endothelium. ECs differ in morphology, function, and gene expression profile, so that even neighbouring cells from the same organ and blood vessel type exhibit distinct features [4]. For instance, vascular ECs may vary in size, shape, thickness and position of the nucleus. Albeit oriented along direction of blood flow, to attenuate the impact of shear stress forces on the vascular wall, microvascular ECs are rather thin (0.1 µm) and spindle-like, whilst their macrovascul...

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H₂S contributes to the hepatic arterial buffer response and mediates vasorelaxation of the hepatic artery via activation of K_ATP channels

Abstract: Siebert N, Cantré D, Eipel C, Vollmar B. H2S contributes to the hepatic arterial buffer response and mediates vasorelaxation of the hepatic artery via activation of KATP channels.

Cited by 64 publications

References 33 publications

Arecoline improves vascular endothelial function in high fructose-fed rats via increasing cystathionine-γ-lyase expression and activating KATP channels

Arecoline improves vascular endothelial function in high fructose-fed rats via increasing cystathionine-γ-lyase expression and activating KATP channels

Taurine Supplementation Lowers Blood Pressure and Improves Vascular Function in Prehypertension

Hydrogen Sulfide and Endothelial Dysfunction: Relationship with Nitric Oxide

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