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      The Role of Hydrogen Sulfide on Cardiovascular Homeostasis: An Overview with Update on Immunomodulation

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          Abstract

          Hydrogen sulfide (H 2S), the third endogenous gaseous signaling molecule alongside nitric oxide (NO) and carbon monoxide, is synthesized by multiple enzymes in cardiovascular system. Similar to other gaseous mediators, H 2S has demonstrated a variety of biological activities, including anti-oxidative, anti-apoptotic, pro-angiogenic, vasodilating capacities and endothelial NO synthase modulating activity, and regulates a wide range of pathophysiological processes in cardiovascular disorders. However, the underlying mechanisms by which H 2S mediates cardiovascular homeostasis are not fully understood. This review focuses on the recent progress on functional and mechanistic aspects of H 2S in the inflammatory and immunoregulatory processes of cardiovascular disorders, importantly myocardial ischemia, heart failure, and atherosclerosis. Moreover, we highlight the challenges for developing H 2S-based therapy to modulate the pathological processes in cardiovascular diseases. A better understanding of the immunomodulatory and biochemical functions of H 2S might provide new therapeutic strategies for these cardiovascular diseases.

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          H2S as a physiologic vasorelaxant: hypertension in mice with deletion of cystathionine gamma-lyase.

          Guangdong Yang, Lingyun Wu, Bo Jiang … (2008)
          Studies of nitric oxide over the past two decades have highlighted the fundamental importance of gaseous signaling molecules in biology and medicine. The physiological role of other gases such as carbon monoxide and hydrogen sulfide (H2S) is now receiving increasing attention. Here we show that H2S is physiologically generated by cystathionine gamma-lyase (CSE) and that genetic deletion of this enzyme in mice markedly reduces H2S levels in the serum, heart, aorta, and other tissues. Mutant mice lacking CSE display pronounced hypertension and diminished endothelium-dependent vasorelaxation. CSE is physiologically activated by calcium-calmodulin, which is a mechanism for H2S formation in response to vascular activation. These findings provide direct evidence that H2S is a physiologic vasodilator and regulator of blood pressure.
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            Two's company, three's a crowd: can H2S be the third endogenous gaseous transmitter?

            Rui Wang (2002)
            Bearing the public image of a deadly "gas of rotten eggs," hydrogen sulfide (H2S) can be generated in many types of mammalian cells. Functionally, H2S has been implicated in the induction of hippocampal long-term potentiation, brain development, and blood pressure regulation. By acting specifically on KATP channels, H2S can hyperpolarize cell membranes, relax smooth muscle cells, or decrease neuronal excitability. The endogenous metabolism and physiological functions of H2S position this gas well in the novel family of endogenous gaseous transmitters, termed "gasotransmitters." It is hypothesized that H2S is the third endogenous signaling gasotransmitter, besides nitric oxide and carbon monoxide. This positioning of H2S will open an exciting field-H2S physiology-encompassing realization of the interaction of H2S and other gasotransmitters, sulfurating modification of proteins, and the functional role of H2S in multiple systems. It may shed light on the pathogenesis of many diseases related to the abnormal metabolism of H2S.
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              The vasorelaxant effect of H(2)S as a novel endogenous gaseous K(ATP) channel opener.

              W Zhao, J ZHANG, Y. Lu … (2001)
              Hydrogen sulfide (H(2)S) has been traditionally viewed as a toxic gas. It is also, however, endogenously generated from cysteine metabolism. We attempted to assess the physiological role of H(2)S in the regulation of vascular contractility, the modulation of H(2)S production in vascular tissues, and the underlying mechanisms. Intravenous bolus injection of H(2)S transiently decreased blood pressure of rats by 12- 30 mmHg, which was antagonized by prior blockade of K(ATP) channels. H(2)S relaxed rat aortic tissues in vitro in a K(ATP) channel-dependent manner. In isolated vascular smooth muscle cells (SMCs), H(2)S directly increased K(ATP) channel currents and hyperpolarized membrane. The expression of H(2)S-generating enzyme was identified in vascular SMCs, but not in endothelium. The endogenous production of H(2)S from different vascular tissues was also directly measured with the abundant level in the order of tail artery, aorta and mesenteric artery. Most importantly, H(2)S production from vascular tissues was enhanced by nitric oxide. Our results demonstrate that H(2)S is an important endogenous vasoactive factor and the first identified gaseous opener of K(ATP) channels in vascular SMCs.
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                Author and article information

                Contributors
                Journal
                Journal ID (nlm-ta): Front Pharmacol
                Journal ID (iso-abbrev): Front Pharmacol
                Journal ID (publisher-id): Front. Pharmacol.
                Title: Frontiers in Pharmacology
                Publisher: Frontiers Media S.A.
                ISSN (Electronic): 1663-9812
                Publication date (Electronic): 26 September 2017
                Publication date Collection: 2017
                Volume: 8
                Electronic Location Identifier: 686
                Affiliations
                [1] 1Department of Pharmacology, School of Pharmacy, Fudan University , Shanghai, China
                [2] 2State Key Laboratory of Quality Research in Chinese Medicine and School of Pharmacy, Macau University of Science and Technology , Macau, China
                Author notes

                Edited by: Jinsong Bian, National University of Singapore, Singapore

                Reviewed by: Hongfang Jin, Peking University First Hospital, China; Yong Ji, Nanjing Medical University, China

                *Correspondence: Xin-Hua Liu, liuxinhua@ 123456fudan.edu.cn Yi-Zhun Zhu, yzzhu@ 123456must.edu.mo

                This article was submitted to Experimental Pharmacology and Drug Discovery, a section of the journal Frontiers in Pharmacology

                Article
                DOI: 10.3389/fphar.2017.00686
                PMC ID: 5622958
                PubMed ID: 29018349
                SO-VID: 6e99fa39-5b98-495f-afe3-0c8b9e638f8c
                Copyright © Copyright © 2017 Pan, Qin, Liu and Zhu.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                Date received : 21 May 2017
                Date accepted : 13 September 2017
                Page count
                Figures: 4, Tables: 0, Equations: 0, References: 116, Pages: 14, Words: 0
                Funding
                Funded by: National Natural Science Foundation of China 10.13039/501100001809
                Award ID: 81330080
                Award ID: 81573420
                Award ID: 81673428
                Categories
                Subject: Pharmacology
                Subject: Review

                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: myocardial ischemia,heart failure,atherosclerosis,inflammation,hydrogen sulfide
                Data availability:
                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: myocardial ischemia, heart failure, atherosclerosis, inflammation, hydrogen sulfide

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