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      The Interaction of the Endogenous Hydrogen Sulfide and Oxytocin Systems in Fluid Regulation and the Cardiovascular System

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          Abstract

          The purpose of this review is to explore the parallel roles and interaction of hydrogen sulfide (H 2S) and oxytocin (OT) in cardiovascular regulation and fluid homeostasis. Their interaction has been recently reported to be relevant during physical and psychological trauma. However, literature reports on H 2S in physical trauma and OT in psychological trauma are abundant, whereas available information regarding H 2S in psychological trauma and OT in physical trauma is much more limited. This review summarizes recent direct and indirect evidence of the interaction of the two systems and their convergence in downstream nitric oxide-dependent signaling pathways during various types of trauma, in an effort to better understand biological correlates of psychosomatic interdependencies.

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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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            Hydrogen sulfide and cell signaling.

            Ling Li, Peter Rose, Philip Moore (2011)
            Hydrogen sulfide (H₂S) is a gaseous mediator synthesized from cysteine by cystathionine γ lyase (CSE) and other naturally occurring enzymes. Pharmacological experiments using H₂S donors and genetic experiments using CSE knockout mice suggest important roles for this vasodilator gas in the regulation of blood vessel caliber, cardiac response to ischemia/reperfusion injury, and inflammation. That H₂S inhibits cytochrome c oxidase and reduces cell energy production has been known for many decades, but more recently, a number of additional pharmacological targets for this gas have been identified. H₂S activates K(ATP) and transient receptor potential (TRP) channels but usually inhibits big conductance Ca²(+)-sensitive K(+) (BK(Ca)) channels, T-type calcium channels, and M-type calcium channels. H₂S may inhibit or activate NF-κB nuclear translocation while affecting the activity of numerous kinases including p38 mitogen-activated protein kinase (p38 MAPK), extracellular signal-regulated kinase (ERK), and Akt. These disparate effects may be secondary to the well-known reducing activity of H₂S and/or its ability to promote sulfhydration of protein cysteine moieties within the cell.
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              Emergence of hydrogen sulfide as an endogenous gaseous signaling molecule in cardiovascular disease.

              David J. Polhemus, David J. Lefer (2014)
              Long recognized as a malodorous and highly toxic gas, recent experimental studies have revealed that hydrogen sulfide (H2S) is produced enzymatically in all mammalian species including man and exerts several critical actions to promote cardiovascular homeostasis and health. During the past 15 years, scientists have determined that H2S is produced by 3 endogenous enzymes and exerts powerful effects on endothelial cells, smooth muscle cells, inflammatory cells, mitochondria, endoplasmic reticulum, and nuclear transcription factors. These effects have been reported in multiple organ systems, and the majority of data clearly indicate that H2S produced by the endogenous enzymes exerts cytoprotective actions. Recent preclinical studies investigating cardiovascular diseases have demonstrated that the administration of physiological or pharmacological levels of H2S attenuates myocardial injury, protects blood vessels, limits inflammation, and regulates blood pressure. H2S has emerged as a critical cardiovascular signaling molecule similar to nitric oxide and carbon monoxide with a profound effect on the heart and circulation. Our improved understanding of how H2S elicits protective actions, coupled with the rapid development of novel H2S-releasing agents, has resulted in heightened enthusiasm for the clinical translation of this ephemeral gaseous molecule. This review will examine our current state of knowledge about the actions of H2S within the cardiovascular system with an emphasis on the therapeutic potential and molecular cross talk between H2S, nitric oxide, and carbon monoxide.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Antioxidants (Basel)
                Journal ID (iso-abbrev): Antioxidants (Basel)
                Journal ID (publisher-id): antioxidants
                Title: Antioxidants
                Publisher: MDPI
                ISSN (Electronic): 2076-3921
                Publication date (Electronic): 14 August 2020
                Publication date Collection: August 2020
                Volume: 9
                Issue: 8
                Electronic Location Identifier: 748
                Affiliations
                [1 ]Clinic for Psychosomatic Medicine and Psychotherapy, Ulm University Medical Center, 89081 Ulm, Germany; nicole.denoix@ 123456uni-ulm.de
                [2 ]Institute for Anesthesiological Pathophysiology and Process Engineering, Ulm University Medical Center, 89081 Ulm, Germany; sarah.ecker@ 123456uni-ulm.de (S.E.); peter.radermacher@ 123456uni-ulm.de (P.R.); tamara.merz@ 123456uni-ulm.de (T.M.)
                [3 ]Faculty of Science, York University, Toronto, ON M3J 1P3, Canada; ruiwang@ 123456yorku.ca
                [4 ]Department of Psychosomatic Medicine and Psychotherapy, Nuremberg General Hospital, Paracelsus Medical University, 90419 Nuremberg, Germany; christiane.waller@ 123456klinikum-nuernberg.de
                Author notes
                Author information
                https://orcid.org/0000-0001-7879-7695
                https://orcid.org/0000-0002-5519-9171
                Article
                Publisher ID: antioxidants-09-00748
                DOI: 10.3390/antiox9080748
                PMC ID: 7465147
                PubMed ID: 32823845
                SO-VID: 06700bee-a476-4cc4-b81e-d38cabea85de
                Copyright © © 2020 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 06 July 2020
                Date accepted : 11 August 2020
                Categories
                Subject: Perspective

                Keywords: cystathionine γ-lyase,hydrogen sulfide,oxytocin receptor,psychosomatic medicine,cardiovascular,fluid regulation
                Data availability:
                Keywords: cystathionine γ-lyase, hydrogen sulfide, oxytocin receptor, psychosomatic medicine, cardiovascular, fluid regulation

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