The Experts below are selected from a list of 4092 Experts worldwide ranked by ideXlab platform
Rui Wang - One of the best experts on this subject based on the ideXlab platform.
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Golgi Stress Response, Hydrogen Sulfide Metabolism, and Intracellular Calcium Homeostasis.
Antioxidants & redox signaling, 2020Co-Authors: Yanjie Zhang, Rui Wang, Yanxi Pei, Yuehong Wang, Ethan Read, Guangdong YangAbstract:Aims: The physiological and pathological importance of hydrogen sulfide (H2S) as a novel Gasotransmitter has been widely recognized. Cystathionine gamma-lyase (CSE) is one of the major H2S-producin...
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Chapter 1:Overview of Gasotransmitters and the Related Signaling Network
Metallobiology, 2018Co-Authors: Rui WangAbstract:The first Gasotransmitter, NO, was discovered in 1977. Twenty-five years later, the Gasotransmitter family was conceptualized. It took another 15 years for the expansion of the Gasotransmitter family to include NO, CO, H2S, and NH3. What are Gasotransmitters? Why should we use this specific nomenclature? Why are Gasotransmitters important in our body? These interesting questions are answered in detail in this chapter. Further discussions are elaborated to clarify the Gasotransmitter signaling network in eukaryotes with a focus on four interaction nodes: the interaction of Gasotransmitters with their producers, interaction of Gasotransmitters with their users/targets, interaction of Gasotransmitters with their sensors, and the interactions between Gasotransmitters themselves. The high tide of Gasotransmitter research has arrived and it is up to researchers to take advantage of such a rewarding surf odyssey.
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Gasotransmitters: growing pains and joys
Trends in biochemical sciences, 2014Co-Authors: Rui WangAbstract:Gasotransmitters are endogenously generated molecules of gas. Over the past decade we have come to realize that these gaseous signaling molecules are crucially important, being irreplaceable in wide biological applications. However, there are still many challenges for future Gasotransmitter research to tackle. These include clarifying the interactions among Gasotransmitters; understanding the significance of the cellular Gasotransmitter signaling network; and adding new members to the modern family of Gasotransmitters in addition to nitric oxide (NO), carbon monoxide (CO), and hydrogen sulfide (H2S). Ammonia fulfills all criteria for being a Gasotransmitter, and methane is another conceivable candidate. Following the original article postulating the concept of multiple Gasotransmitters over a decade ago, this sequel article aims to further inspire interest and exploration into Gasotransmitter research.
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S1-2 The next wave of Gasotransmitter research
Nitric Oxide, 2014Co-Authors: Rui WangAbstract:Gasotransmitters are endogenously generated molecules of gas. They are freely permeable to cell membranes and their effects do no depend on specific membrane receptors or second messengers. These gaseous signaling molecules functions at physiologically relevant concentrations. The concept of “Gasotransmitter” opens new windows for understanding the complex and interweaved cellular signaling networks. Wide application and critical biological importance of Gasotransmitters have been realized over the last decade. Nitric oxide (NO) is produced from l -arginine. Carbon monoxide (CO) is a product of heme metabolism and regulates numerous physiological processes as NO does. Hydrogen sulfide (H2S) is the third Gasotransmitter in terms of its discovery chronology relative to that of NO and CO. While NO takes the role of an endothelium-derived relaxing factor (EDRF), H2S fills the gap as an endothelium-derived hyperpolarizing factor (EDHF). These are examples of the physiological and pathophysiological roles of Gasotransmitters. Gasotransmitter are biologically irreplaceable. They SAVE life. The challenges for future Gasotransmitter research are plentiful. One of them is the complexity of the interactions among Gasotransmitters and the significance of their cross-talks for cellular signaling network. Gasotransmitters share many common molecular targets but modulate their activities through different mechanisms. They also act on different targets but affect the common outcome. Finally, guess who’s coming to dinner as new member (s) of the modern family of Gasotransmitters. The next wave of Gasotransmitter research will be as big as one can envisage – you can take my prediction to the bank. (Supported by Canadian Institutes of Health Research).
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Shared signaling pathways among Gasotransmitters.
Proceedings of the National Academy of Sciences of the United States of America, 2012Co-Authors: Rui WangAbstract:Gasotransmitters, including NO, CO, and H2S, are a group of endogenously produced gas molecules that are membrane-permeable and share similar molecular targets (1). Gasotransmitters may antagonize or potentiate each other’s cellular effects at three levels: their production, their downstream molecular targets, and the direct chemical interaction among themselves. The study published in PNAS by Coletta et al. (2) presents an interesting example of how the interaction of Gasotransmitters converges at the same downstream molecular target. Coletta et al. found that the proangiogenic effect of H2S on angiogenesis and wound healing was completely absent in endothelial NO synthase KO mice, and that eliminating H2S production by silencing cystathionine-γ-lyase (CSE) abolished NO-stimulated angiogenesis (2). This mutually dependent relationship between H2S and NO in vascular endothelial cells is rooted in the regulation of the cellular levels of cGMP. NO activates soluble guanylyl cyclase (sGC) to generate cGMP, whereas H2S inhibits phosphodiesterase-5 (PDE5) to slow down the degradation of the existing cGMP (2). A net increase in cGMP level leads to the activation of protein kinase G (PKG) and its downstream effector, vasodilator-stimulated phosphoprotein. Lack of NO might curtail the production of cGMP so that H2S-inhibited cGMP degradation becomes meaningless. Conversely, rapid degradation of the existing cGMP in the absence of H2S would render NO powerless to elicit angiogenesis.
Solomon H. Snyder - One of the best experts on this subject based on the ideXlab platform.
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Gasotransmitter hydrogen sulfide signaling in neuronal health and disease
Biochemical Pharmacology, 2018Co-Authors: Bindu D Paul, Solomon H. SnyderAbstract:Hydrogen sulfide is a gaseous signaling molecule or Gasotransmitter which plays important roles in a wide spectrum of physiologic processes in the brain and peripheral tissues. Unlike nitric oxide and carbon monoxide, the other major Gasotransmitters, research on hydrogen sulfide is still in its infancy. One of the modes by which hydrogen sulfide signals is via a posttranslational modification termed sulfhydration/persulfidation, which occurs on reactive cysteine residues on target proteins, where the reactive –SH group is converted to an –SSH group. Sulfhydration is a substantially prevalent modification, which modulates the structure or function of proteins being modified. Thus, precise control of endogenous hydrogen sulfide production and metabolism is critical for maintenance of optimal cellular function, with excess generation and paucity, both contributing to pathology. Dysregulation of the reverse transsulfuration pathway which generates hydrogen sulfide occurs in several neurodegenerative diseases such as Parkinson's disease, Huntington's disease and Alzheimer's disease. Accordingly, treatment with donors of hydrogen sulfide or stimulation of the reverse transsulfuration have proved beneficial in several neurodegenerative states. In this review we focus on hydrogen sulfide mediated neuronal signaling processes that contribute to neuroprotection.
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Hydrogen sulfide: A Gasotransmitter of clinical relevance
Journal of Molecular Medicine, 2012Co-Authors: M. Scott Vandiver, Solomon H. SnyderAbstract:Though the existence of hydrogen sulfide (H2S) in biological tissues has been known for over 300 years, it is the most recently appreciated of the Gasotransmitters as a physiologic messenger molecule. The enzymes cystathionine γ-lyase (CSE) and cystathionine β-synthase (CBS) had long been speculated to generate H2S, and inhibitors of these enzymes had been employed to characterize influences of H2S in various organs. Definitive evidence that H2S is a physiologic regulator came with the development of mice with targeted deletion of CSE and CBS. Best characterized is the role of H2S, formed by CSE, as an endothelial derived relaxing factor that normally regulates blood pressure by acting through ATP-sensitive potassium channels. H2S participates in various phases of the inflammatory process, predominantly exerting anti-inflammatory actions. Currently, the most advanced efforts to develop therapeutic agents involve the combination of H2S donors with non-steroidal anti-inflammatory drugs (NSAIDs). The H2S releasing moiety provides cytoprotection to gastric mucosa normally adversely affected by NSAIDs while the combination of H2S and inhibition of prostaglandin synthesis may afford synergistic anti-inflammatory influences.
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Protein modifications involved in neurotransmitter and Gasotransmitter signaling
Trends in neurosciences, 2010Co-Authors: Nilkantha Sen, Solomon H. SnyderAbstract:Covalent modifications of intracellular proteins, such as phosphorylation, are generally thought to occur as secondary or tertiary responses to neurotransmitters, following the intermediation of membrane receptors and second messengers such as cyclic AMP. By contrast, the Gasotransmitter nitric oxide directly S-nitrosylates cysteine residues in diverse intracellular proteins. Recently, hydrogen sulfide has been acknowledged as a Gasotransmitter, which analogously sulfhydrates cysteine residues in proteins. Cysteine residues are also modified by palmitoylation in response to neurotransmitter signaling, possibly in reciprocity with S-nitrosylation. Neurotransmission also elicits sumoylation and acetylation of lysine residues within diverse proteins. This review addresses how these recently appreciated protein modifications impact our thinking about ways in which neurotransmission regulates intracellular protein disposition.
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hydrogen sulfide as a Gasotransmitter
Journal of Neurochemistry, 2010Co-Authors: Moataz M Gadalla, Solomon H. SnyderAbstract:Nitric oxide (NO) and carbon monoxide (CO) are well established as messenger molecules throughout the body, Gasotransmitters, based on striking alterations in mice lacking the appropriate biosynthetic enzymes. Hydrogen sulfide (H2S) is even more chemically reactive, but till recently there was little definitive evidence for its physiologic formation. Cystathionine β-synthase (CBS, EC 4.2.1.22), and Cystathionine γ-lyase (CSE; EC 4.4.1.1), also known as cytathionase, can generate H2S from cyst(e)ine. Very recent studies with mice lacking these enzymes have established that CSE is responsible for H2S formation in the periphery, while in the brain CBS is the biosynthetic enzyme. Endothelial-derived relaxing factor (EDRF) activity is reduced 80% in the mesenteric artery of mice with deletion of CSE, establishing H2S as a major physiologic EDRF. H2S appears to signal predominantly by S-sulfhydrating cysteines in its target proteins, analogous to S-nitrosylation by NO. Whereas S-nitrosylation typically inhibits enzymes, S-sulfhydration activates them. S-nitrosylation basally affects 1–2% of its target proteins, while 10–25% of H2S target proteins are S-sulfhydrated. In summary, H2S appears to be a physiologic Gasotransmitter of comparable importance to NO and CO.
Michael G. Sarr - One of the best experts on this subject based on the ideXlab platform.
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hydrogen sulfide modulates contractile function in rat jejunum
Journal of Surgical Research, 2012Co-Authors: Michael S. Kasparek, David R. Linden, Gianrico Farrugia, Michael G. SarrAbstract:After nitric oxide (NO) and carbon monoxide (CO) were identified as gas “transmitters”, hydrogen sulfide (H2S) was identified as the third “Gasotransmitter” [1]. Because Gasotransmitters are freely permeable across cell membranes and NO and CO act on intracellular targets, Gasotransmitters offer a new paradigm to classic signal transduction by neuronally released “neurotransmitters” which act via membrane-bound receptors. Intracellular mechanisms of signaling are well-studied for NO and CO, but mechanisms mediating effects of H2S are not understood in gastrointestinal tissues. H2S has been well studied in vascular smooth muscle, where H2S opens ATP-sensitive K+-channels causing hyperpolarization, closing of voltage-gated Ca2+-channels, and muscular relaxation [1,2]. In gastrointestinal smooth muscle, the other Gasotransmitters NO and CO, released from the enteric nervous system (ENS), suppress contractile activity. Evidence suggests that H2S is an endogenous Gasotransmitter capable of suppressing contractile activity in the gut. Cystathionine-β-synthase (CBS) and cystathionine-γ-lyase (CSE), enzymes which catalyze endogenous production of H2S from L-cysteine [1], are co-expressed in submucous and myenteric plexuses of guinea pig colon and submucous plexus of human colon [3]. Guinea pig ileum incubated with L-cysteine has been reported to generate H2S that is inhibited by antagonists of CBS [4]. In vascular smooth muscle, NO interacts with H2S by amplifying the relaxant effects of H2S, stimulating the activity of CSE, and increasing expression of CSE [2,4-6]. In other tissues, several studies with H2S show excitation of primary afferent nerve fibers in stimulating Cl−-secretion from guinea pig and human colon by an axon reflex [3] and “pro-contractile” effects in rat bladder [7] and guinea pig airways [8]. In the gut, mechanisms of H2S in modulating contractile activity are not understood. In mouse and human colon, H2S suppresses spontaneous contractile activity via ATP-sensitive K+ channels, these effects are inhibited by glibenclamine [9], In guinea pig antrum, concentrations of H2S (<0.3 mM NaHS) increase muscle tension and decrease contractile amplitude; greater concentrations of HsS suppress contractile amplitude but do not affect tension [10]. Both effects appear mediated by potassium channels. Two studies using rat, rabbit, and guinea pig ileum suggested an inhibitory effect of H2S on contractile activity independent of ATP-sensitive K+ channels [4,5]. Gallego et al [9] found suppression of spontaneous activity in mouse jejunum by H2S that was unaffected by inhibiting nitric oxide synthase, neuronal activity by tetrodotoxin, purinergic receptors by PPADS, or primary visceral afferent nerves by capsaicin. The role of potassium channels is not well studied as in stomach [10] and colon [9]. The role of HsS in the control of longitudinal muscle contractility is also not well studied. Our aim was to determine effects of exogenously applied and endogenously released H2S in rat intestinal smooth muscle. We studied jejunal longitudinal muscle as part of our systematic approach to understanding inhibitory neurotransmitters in all muscular layers of the small intestine. By using targeted antagonists, we explored involvement of the ENS, primary afferent nerve fibers, NO, and direct effects on smooth muscle in the response to H2S. We also evaluated exogenously applied L-cysteine as the substrate for endogenous H2S production and explored expression of CBS and CSE immunohistochemically. Our hypothesis was that H2S acts as an endogenous suppressor of contractile activity in rat jejunal smooth muscle by a direct effect on smooth muscle.
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ROLE OF HYDROGEN SULFIDE AS A Gasotransmitter IN MODULATING CONTRACTILE ACTIVITY OF CIRCULAR MUSCLE OF RAT JEJUNUM
Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract, 2011Co-Authors: Munenori Nagao, Judith A. Duenes, Michael G. SarrAbstract:Aim Our aim was to determine mechanisms of action of the Gasotransmitter hydrogen sulfide (H2S) on contractile activity in circular muscle of rat jejunum.
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Mechanisms of Action of the Gasotransmitter Hydrogen Sulfide in Modulating Contractile Activity of Longitudinal Muscle of Rat Ileum
Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract, 2010Co-Authors: Munenori Nagao, David R. Linden, Judith A. Duenes, Michael G. SarrAbstract:Aim This study aims to determine mechanisms of action of the Gasotransmitter hydrogen sulfide (H2S) on contractile activity in longitudinal muscle of rat ileum.
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Gasotransmitters in the gastrointestinal tract
Surgery, 2008Co-Authors: Michael S. Kasparek, David R. Linden, Martin E. Kreis, Michael G. SarrAbstract:The 1990s initiated a new paradigm for cell-to-cell signal transduction via “neurotransmitters” with the discovery that a gas, nitric oxide (NO), could be released specifically from nerves and act to transmit the “neural signal” secondary to nerve stimulation. But, unlike the classic paradigm of a neurotransmitter being released extracellularly from prestored vesicles and binding to a membrane-bound receptor on the effector cell, NO is synthesized on demand from nitric oxide synthase (NOS) (rather than stored in vesicles), then released extracellularly, and diffuses across the cell membrane to act on an intracellular enzyme guanylate cyclase to transduce the primary neural signal. The recognition of carbon monoxide (CO) soon followed as a second gaseous neurotransmitter acting similarly to NO. With the recent acknowledgement of hydrogen sulfide (H2S) as the third gaseous neurotransmitter, the term “Gasotransmitter” was introduced to characterize gases which act as neurally released transmitters1. NO, CO, and H2S share distinct properties, which qualify them as Gasotransmitters in that they 1) are small molecules of gas; 2) are freely permeable across membranes and do not act via specific membrane receptors; 3) are synthesized endogenously and enzymatically on demand and their generation is regulated; 4) have well-defined specific functions at physiologically relevant concentrations; and 5) their cellular effects may or may not be mediated by second messengers, but these Gasotransmitters have specific cellular and molecular targets. Due to their gaseous nature, NO, CO, and H2S are not stored within the cell in the classic presynaptic vesicles before they are released, but rather they are synthesized and released on demand, which distinguishes these Gasotransmitters from classic neurotransmitters such as acetylcholine, norepinephrine, and even the peptide neurotransmitters. Although storage vesicles for Gasotransmitters have not yet been identified, protein adducts might in theory serve as storage pools. Furthermore, presynaptic re-uptake of these released Gasotransmitters, as occurs with other neurotransmitters, has not been described. Gasotransmitters are rapidly scavenged or enzymatically degraded after their release to terminate their signaling activity, with biologic half-lives on the order of seconds. An additional property shared by the three Gasotransmitters is their potential systemic toxicity at supra-physiologic concentrations, which led to the recognition of these gases as air pollutants and toxins before their important in vivo functions were identified or even imagined. Our understanding of the wide spectrum of physiologic functions of each Gasotransmitter in different organ systems continues to grow. This short review will provide an overview about the role of the three established Gasotransmitters, NO, CO, and H2S, focusing primarily on the control of contractile function of the gastrointestinal (GI) tract. We will also address, albeit briefly, their involvement in other important functions, such as inflammation, ileus, pain perception, and carcinogenesis in which they act, not as neurotransmitters, but more as paracrine or even systemically active substances. The number of Gasotransmitters might increase with the addition of such candidate gases as ammonia and acetaldehyde; however, because these gases have not fully met the criteria to classify them as Gasotransmitters, we will focus on the three established Gasotransmitters NO, CO, and H2S for the purpose of this review.
Guangdong Yang - One of the best experts on this subject based on the ideXlab platform.
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Gasotransmitter signaling in energy homeostasis and metabolic disorders.
Free radical research, 2020Co-Authors: Amr Ali, Yuehong Wang, Guangdong YangAbstract:Gasotransmitters are small molecules of gases, including nitric oxide (NO), hydrogen sulfide (H2S), and carbon monoxide (CO). These three Gasotransmitters can be endogenously produced and regulate a wide range of pathophysiological processes by interacting with specific targets upon diffusion in the biological media. By redox and epigenetic of various physiological functions, NO, H2S, and CO are critical for maintenance of intracellular energy homeostasis. Accumulated evidence has shown that these three Gasotransmitters control ATP generation, mitochondrial biogenesis, glucose metabolism, insulin sensitivity, lipid metabolism, and thermogenesis, etc. Abnormal generation and metabolism of NO, H2S, and/or CO are involved in various abnormal metabolic diseases, including obesity, diabetes, and dyslipidemia. In this review, we summarized the roles of NO, H2S, and CO in the regulation of energy homeostasis as well as their involvements in the metabolism dysfunction-related diseases. Understanding the interaction among these Gasotransmitters and their specific molecular targets are very important for therapeutic applications.
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Gasotransmitter signaling in energy homeostasis and metabolic disorders
Free Radical Research, 2020Co-Authors: Amr Ali, Yuehong Wang, Guangdong YangAbstract:Gasotransmitters are small molecules of gases, including nitric oxide (NO), hydrogen sulfide (H2S), and carbon monoxide (CO). These three Gasotransmitters can be endogenously produced and regulate ...
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Golgi Stress Response, Hydrogen Sulfide Metabolism, and Intracellular Calcium Homeostasis.
Antioxidants & redox signaling, 2020Co-Authors: Yanjie Zhang, Rui Wang, Yanxi Pei, Yuehong Wang, Ethan Read, Guangdong YangAbstract:Aims: The physiological and pathological importance of hydrogen sulfide (H2S) as a novel Gasotransmitter has been widely recognized. Cystathionine gamma-lyase (CSE) is one of the major H2S-producin...
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Gasotransmitters in Biology and Medicine: Molecular Mechanisms and Drug Targets.
Oxidative medicine and cellular longevity, 2016Co-Authors: Guangdong Yang, Yanxi Pei, Alp Sener, Michael D PluthAbstract:In the past two decades, an increasing number of reports have indicated the remarkable roles of Gasotransmitters in biology and medicine. The term Gasotransmitter was first coined by Wang in 2002 and further refined in 2012 and 2014 to encompass a group of small gaseous molecules, including nitric oxide (NO), hydrogen sulfide (H2S), carbon monoxide (CO), and possibly other gases [1–3]. A Gasotransmitter typically has high lipid solubility and can penetrate cell membranes without requiring a specific transporter or receptor. Gasotransmitters are generated endogenously by specific enzymes and can generate various functions at physiologically relevant concentrations by targeting specific cellular and molecular targets. Abnormal generation and metabolism of these Gasotransmitters have been extensively demonstrated to be linked to diverse biological processes, such as vascular biology, immune functions, cellular survival, metabolism, longevity, and development and stress resistance.
Chao-shu Tang - One of the best experts on this subject based on the ideXlab platform.
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The regulatory effect of endogenous hydrogen sulfide on pulmonary vascular structure and Gasotransmitters in rats with high pulmonary blood flow.
Life sciences, 2007Co-Authors: Hongfang Jin, Xiuying Tang, Chao-shu TangAbstract:Abstract The study aimed to explore the regulatory effect of endogenous hydrogen sulfide (H2S), a novel Gasotransmitter, on pulmonary vascular structure and Gasotransmitters in rats with high pulmonary blood flow. Thirty-two Sprague–Dawley rats were randomly divided into a sham group, shunt group, sham + PPG (propargylglycine, an inhibitor of cystathionine-γ-lyase) group and shunt + PPG group. Rats in the shunt and shunt + PPG groups underwent abdominal aorta–inferior vena cava shunting. Rats in the shunt + PPG and sham + PPG groups were intraperitoneally injected with PPG. After 4 weeks of shunting, mean pulmonary artery pressure (MPAP) and pulmonary vascular structural remodeling (PVSR) were evaluated. H2S, nitric oxide (NO) and carbon monoxide (CO) contents were measured in lung tissues. Meanwhile, nitric oxide synthase (eNOS), heme oxygenase (HO-1) and proliferative cell nuclear antigen (PCNA) protein expressions and ERK activation were evaluated. After 4 weeks of shunting, rats showed PVSR with increased lung tissue H2S and NO content but decreased CO content. After the PPG treatment, MPAP further increased and PVSR was aggravated. Meanwhile, PCNA expression and ERK activation were augmented with decreased lung tissue CO and HO-1 protein production but increased lung tissue NO production and eNOS expression. H2S exerted a protective effect on PVSR, and the inhibition of the NO/NOS pathway and the augmentation of the CO/HO pathway might be involved in the mechanisms by which H2S regulates PVSR in rats with high pulmonary flow.
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Role of Gasotransmitters in the pathogenesis of pulmonary hypertension
Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences, 2006Co-Authors: Yan-fei Wang, Hongfang Jin, Chao-shu TangAbstract:Pulmonary hypertension is a complicated and important pathological process in the development of a variety of cardiovascular and pulmonary diseases, and directly affects the development of the diseases and their prognosis. but its mechanisms are still not fully understood. Therefore, to clarify the mechanisms is an important task in this field. Nitric oxide (NO) and carbon monoxide (CO) have special significance in pulmonary circulation as compared with other organs for their special biological properties including continuous production, fast transmission and extensive action, etc, which attracts great attention in the life science research and initiates the new research field of Gasotransmitters. Hydrogen sulfide (H2S), which has been recognized as a toxic gas, can be endogenously produced in the body. We considered it to be a new cardiovascular regulatory Gasotransmitter based on the studies of its synthesis and distribution in cardiovascular system and cardiovascular effects under physiologic and pathophysiologic conditions. We found it exerted a general regulatory significance in cardiovascular diseases. Based on the research of the three Gasotransmitters in hypoxic and high pulmonary blood flow-induced pulmonary hypertension, it was found that the dysfunction of the Gasotransmitter pathways was involved in the pathogenesis of pulmonary hypertension and the supplement of Gasotransmitters could alleviate pulmonary hypertension and pulmonary vascular remodeling. The mechanisms included that they could regulate vessel dilation, correct the imbalance between smooth muscle cell proliferation and apoptosis, inhibit the excess synthesis and stimulate the degradation of collagen, therefore inhibiting abnormal accumulation of collagen, etc. All these results indicated the significant regulatory effects of Gasotransmitters in the pathogenesis of pulmonary hypertension.
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A Newly Found Gasotransmitter, Hydrogen Sulfide, in the Pathogenesis of Hypertension and Other Cardiovascular Diseases
Current Hypertension Reviews, 2006Co-Authors: Chunyu Zhang, Hui Yan, Chao-shu TangAbstract:In the 1980s, nitric oxide (NO) and carbon monoxide (CO) were determined to be gaseous messenger molecules which is capable of relaxing vessels and interfering with vascular structure remodeling. However there are many mechanisms that have not been clear about the regulation of human functions under both physiological and pathophysiological conditions. Hydrogen sulfide (H2S) is a newly found gasotrasmitter that was demonstrated to play similar role as that of NO and CO in many organs and tissues, especially in the cardiovascular system. In this review, firstly, we described the production of H2S in the body, and the functions of H2S in the cardiovascular system, especially in the vascular relaxing and vascular remodeling. Secondly, we further discussed the role of H2S in hypertension, hypoxic pulmonary hypertension, shock and ischemic hear disease. Finally, the interaction between H2S and the other two Gasotransmitters, NO and CO, was also discussed.