Contractile and Vasorelaxant Effects of Hydrogen Sulfide and Its Biosynthesis in the Human Internal Mammary Artery

Webb, G. A.; Lim, Lay Har; Oh, Vernon M S; Yeo, Soh Bee; Cheong, Yoke Ping; Ali, Yusuf; Oakley, Reida El; Lee, Chuen Neng; Wong, Poo Sing; Caleb, Michael George; Salto-Tellez, Manuel; Bhatia, Madhav; Chan, Eng Soon; Taylor, Elizabeth A.; Moore, Philip K.

doi:10.1124/jpet.107.133538

Cited by 142 publications

(134 citation statements)

References 25 publications

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“…Mixing of H 2 S donor NaHS with NO donors (SNP or SNAP) diminished vasorelaxant effect of each NO donor on rat aorta and low concentrations of H 2 S contracted human internal mammary artery (Ali et al 2006;Webb et al 2008). It was suggested that H 2 S was able to inactivate NO by chemical reaction with NO to produce an unidentified nitrosothiol (Ali et al 2006;Whiteman et al 2006;Webb et al 2008). Munro and Williams (2000) supposed nitrosodisulfide ion ONSS -as the result of RSNOs reaction with sulfur-centred nucleophiles.…”

Section: Discussionmentioning

confidence: 99%

The hypothesis of the main role of H2S in coupled sulphide-nitroso signalling pathway

Bertova

Čačányiová²,

Kristek³

et al. 2010

gpb

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Abstract. As a part of the nitroso signalling pathway, nitroso-compounds serve as stores and carriers of NO; as part of the sulphide signalling pathway, bound sulfane-sulphur compounds serve as stores and carriers of H 2 S. Here we hypothesise a coupled sulphide-nitroso signalling pathway, in which H 2 S plays a main role. H 2 S releases NO from the endogenous S-nitroso-compounds nitrosocysteine, nitroso-acetylcysteine and nitroso-albumin. Relaxation of noradrenaline-precontracted aortic rings by H 2 S is also enhanced in the presence of nitroso-albumin, which may implicate the involvement of the nitroso signalling pathway. Pretreatment of albumin, cysteine, N-acetylcysteine and lipids with H 2 S results in binding of sulphur to these compounds creating thus new-modified sulphur compounds that release NO from nitroso-compounds directly and/or through released H 2 S, which suggests sulphide-nitroso signalling pathway participation. This hypothesis is supported by the observation that the pretreatment of noradrenaline-precontracted aortic rings with H 2 S significantly enhanced relaxation induced by nitroso-glutathione in the absence of H 2 S. We assume that the NO release from nitroso-compounds directly by H 2 S or indirectly by the H 2 S-induced sulphur-bound compounds represents coupled sulphide-nitroso signalling, which may explain some of the numerous biological effects of H 2 S that are shared with NO.

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Section: Discussionmentioning

confidence: 99%

The hypothesis of the main role of H2S in coupled sulphide-nitroso signalling pathway

Bertova

Čačányiová²,

Kristek³

et al. 2010

gpb

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“…H 2 S is endogenously produced from L-cysteine predominantly by the enzymes cystathionine-γ-lyase (CSE) and cystathionine-β-synthase (CBS) in a variety of animals, from invertebrates to mammals (Fiorucci et al 2005b;Gainey and Greenberg 2005;Geng et al 2004b;Julian et al 2005;Julian et al 2002;Kimura 2000;Kimura et al 2005;Wang 2002;Webb et al 2008). Recently, 3-mercaptopyruvate sulfurtransferase (3-MST), in conjunction with cysteine aminotransferase, has also been found to produce H 2 S from cysteine (Shibuya et al 2009;Shibuya et al 2008).…”

Section: Introductionmentioning

confidence: 99%

“…Since then a variety of physiological roles have been proposed for H 2 S (Lowicka and Beltowski 2007;Szabo 2007), and at least some capacity for H 2 S production has been demonstrated in several vertebrate tissues Olson 2005;Olson et al 2006;Zhao et al 2003), including human mammary artery (Webb et al 2008). When exogenously applied to isolated blood vessels of vertebrates, H 2 S elicits responses that range from a monophasic relaxation or contraction, to multiphasic contraction-relaxation-contraction responses, depending on the phylogenetic class and type of vessel examined (Dombkowski et al 2005).…”

Section: Introductionmentioning

confidence: 99%

The hydrogen sulfide signaling system: changes during aging and the benefits of caloric restriction

Predmore

Alendy

Ahmed

et al. 2010

AGE

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Hydrogen sulfide gas (H 2 S) is a putative signaling molecule that causes diverse effects in mammalian tissues including relaxation of blood vessels and regulation of perfusion in the liver, but the effects of aging on H 2 S signaling are unknown. Aging has negative impacts on the cardiovascular system. However, the liver is more resilient with age. Caloric restriction (CR) attenuates affects of age in many tissues. We hypothesized that the H 2 S signaling system is negatively affected by age in the vasculature but not in the liver, which is typically more resilient to age, and that a CR diet minimizes the age affect in the vasculature. To investigate this, we determined protein and mRNA expression of the H 2 S-producing enzymes cystathionine γ-lyase (CSE) and cystathionine β-synthase (CBS), H 2 S production rates in the aorta and liver, and the contractile response of aortic rings to exogenous H 2 S. Tissue was collected from Fisher 344×Brown Norway rats from 8-38 months of age, which had been maintained on an ad libitum (AL) or CR diet. The results demonstrate that age and diet have differential effects on the H 2 S signaling system in aorta and liver. The aorta showed a sizeable effect of both age and diet, whereas the liver only showed a sizeable effect of diet. Aortic rings showed increased contractile sensitivity to H 2 S and increased protein expression of CSE and CBS with age, consistent with a decrease in H 2 S concentration with age. CR appears to benefit CSE and CBS protein in both aorta and liver, potentially by reducing oxidative stress and ameliorating the negative effect of age on H 2 S concentration. Therefore, CR may help maintain the H 2 S signaling system during aging.

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“…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]. H 2 S has been shown to dilate other isolated mammalian blood conduits in vitro, such as human internal mammary artery [103], mouse aorta and ear microcirculation [104,105], and newborn pig cerebral arterioles [106]. Consistent with these data, the systemic injection of NaHS at 10-50 activity in VSMCs, which leads to vasorelaxation in a PKG-dependent manner [48,111,112].…”

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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Contractile and Vasorelaxant Effects of Hydrogen Sulfide and Its Biosynthesis in the Human Internal Mammary Artery

Cited by 142 publications

References 25 publications

The hypothesis of the main role of H2S in coupled sulphide-nitroso signalling pathway

The hypothesis of the main role of H2S in coupled sulphide-nitroso signalling pathway

The hydrogen sulfide signaling system: changes during aging and the benefits of caloric restriction

Hydrogen Sulfide and Endothelial Dysfunction: Relationship with Nitric Oxide

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