Abstract

The purpose of this review is to explore the parallel roles and interaction of hydrogen sulfide (H2S) 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 H2S in physical trauma and OT in psychological trauma are abundant, whereas available information regarding H2S 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.

Highlights

  • The gasotransmitter hydrogen sulfide (H2 S) (endogenously produced by cystathionine γ-lyase (CSE), cystathionine β-synthase (CBS) and 3-mercaptopyruvate-sulfurtransferase (3MST)) and the neuroendocrine oxytocin (OT) system have been recently shown to possibly play parallel roles in the heart and the brain in response to trauma, and to influence one another

  • Produced by CSE in the cardiovascular system, and the oxytocin receptor (OTR), stimulated by OT, can both activate the reperfusion injury salvage kinase (RISK) activation leads to PI3K, protein kinase B (Akt), ERK1/2 cascades and endothelial nitric oxide

  • This suggests that multiple factors may be at play in the regulation of the OT system, stress being one of them, affecting endogenous receptor ligand levels and the physiological response

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Summary

Introduction

The gasotransmitter hydrogen sulfide (H2 S) (endogenously produced by cystathionine γ-lyase (CSE), cystathionine β-synthase (CBS) and 3-mercaptopyruvate-sulfurtransferase (3MST) (as depicted in Figure 1)) and the neuroendocrine oxytocin (OT) system have been recently shown to possibly play parallel roles in the heart and the brain in response to trauma, and to influence one another. H2 S can be produced in the vasculature, brain, placenta, colonic tissue, liver, kidney andand other mammalian tissues [8].[8]. Cysteine-aminotransferase (CAT) can metabolize L-cysteine to 3-mercaptopyruvate, which is to H2S by 3MST. Enzymatic H2S generation can take place during hypoxic events, for example, via thiosulfate. Non-enzymatic H2 S generation can take place during hypoxic events, for example, via thiosulfate utilization. Thiosulfate is an oxidation product of H2S, which is part of the stepwise enzymatic sulfide utilization. H2S produced exogenously onset of labor [11]

Sexpression produced locally and exogenously administered administered
The Neuroendocrine Control of Fluid Hemostasis
H2 S in Cardiac and Vascular Protection
Chronic Cardiovascular Disease
Conclusions
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