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

Antioxidants ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 748
Author(s):  
Nicole Denoix ◽  
Oscar McCook ◽  
Sarah Ecker ◽  
Rui Wang ◽  
Christiane Waller ◽  
...  

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.

2011 ◽  
Vol 12 (9) ◽  
pp. 1406-1415 ◽  
Author(s):  
Daniele Mancardi ◽  
Alessandra Florio Pla ◽  
Francesco Moccia ◽  
Franco Tanzi ◽  
Luca Munaron

2016 ◽  
Vol 2016 ◽  
pp. 1-16 ◽  
Author(s):  
B. V. Nagpure ◽  
Jin-Song Bian

Historically acknowledged as toxic gases, hydrogen sulfide (H2S) and nitric oxide (NO) are now recognized as the predominant members of a new family of signaling molecules, “gasotransmitters” in mammals. While H2S is biosynthesized by three constitutively expressed enzymes (CBS, CSE, and 3-MST) from L-cysteine and homocysteine, NO is generated endogenously from L-arginine by the action of various isoforms of NOS. Both gases have been transpired as the key and independent regulators of many physiological functions in mammalian cardiovascular, nervous, gastrointestinal, respiratory, and immune systems. The analogy between these two gasotransmitters is evident not only from their paracrine mode of signaling, but also from the identical and/or shared signaling transduction pathways. With the plethora of research in the pathophysiological role of gasotransmitters in various systems, the existence of interplay between these gases is being widely accepted. Chemical interaction between NO and H2S may generate nitroxyl (HNO), which plays a specific effective role within the cardiovascular system. In this review article, we have attempted to provide current understanding of the individual and interactive roles of H2S and NO signaling in mammalian cardiovascular system, focusing particularly on heart contractility, cardioprotection, vascular tone, angiogenesis, and oxidative stress.


Author(s):  
А.В. Муравьев ◽  
П.В. Михайлов ◽  
И.А. Тихомирова ◽  
Н. Антонова ◽  
А.А. Муравьев

Введение. Эритроциты — высокоспециализированные клетки, основной функцией которых является транспорт кислорода. Они лишены ядра и митохондрий, однако сохранили многие элементы молекулярных сигнальных путей. При выполнении транспортной функции эритроциты изменяют свои механические свойства и в том числе деформируются и объединяются в комплексы — агрегаты. Имеется ряд свидетельств того, что изменение механических свойств эритроцитов происходит под влиянием сигнальных молекул, к которым относятся и газовые медиаторы или газотрансмиттеры (ГТ). Это оксид азота, монооксид углерода и сульфид водорода. Цель исследования: изучение микрореологических ответов человеческих эритроцитов на действие ряда доноров газотрансмиттеров — оксида азота и сульфида водорода. Материалы и методы. После инкубирования эритроцитов с донорами оксида азота (спермином и нитропруссидом натрия) и донором сульфида водорода (гидросульфидом натрия) регистрировали деформируемость эритроцитов, их агрегацию и вязкость суспензий клеток (показатель гематокрита — 40%, вязкость суспензионной среды — 1,30 мПа × с; раствор Рингера и декстран‑200). Для уточнения механизмов действия ГТ на микрореологические свойства эритроцитов их инкубировали с ацетилхолином, серотонином и форсколином. Результаты. Установлено, что под влиянием ГТ происходят заметные изменения микромеханических свойств эритроцитов, которые статистически значимо изменялись под влиянием доноров оксида азота. Более существенные сдвиги микрореологии клеток, особенно их агрегацию, вызывал нитропруссид натрия. Гидросульфид натрия умеренно, но статистически значимо повышал деформируемость эритроцитов и заметно снижал их агрегацию, однако его эффекты уступали действию нитропруссида натрия. Заключение. На основании полученных данных и их анализа можно полагать, что внутриклеточными сигнальными путями для исследованных ГТ в эритроцитах при изменении их микромеханического состояния могут быть как ферменты гуанилатциклаза и аденилатциклаза, так и ионные каналы мембраны клетки. Introduction. Erythrocytes are highly specialized cells; oxygen transport is their main function. They have no nucleus and mitochondria, but they saved many elements of molecular signaling pathways. When erythrocytes performed the transport function they change their mechanical properties, deformed and combined into complexes — aggregates. There are some data that erythrocytes change their mechanical properties under the influence of signaling molecules such as gas mediators or gasotransmitters (GTs) — nitric oxide (NO), carbon monoxide and hydrogen sulfide. Aim: to study the microrheological responses of erythrocytes on the action of number GTs-donors — nitric oxide and hydrogen sulfide. Materials and methods. After erythrocytes incubation with NO-donors (spermine and sodium nitroprusside) and donor of hydrogen sulfide (sodium hydrosulfide) we registered erythrocytes deformability, their aggregation and viscosity of cell suspensions (hematocrit — 40%, viscosity of suspension medium — 1.30 mPa × s; Ringer’s solution and dextran‑200). To clarify the mechanisms of GTs action on microrheological properties of erythrocytes they were incubated with acetylcholine, serotonin and forskolin. Results. GTs noticeably changed erythrocytes micromechanical properties. Sodium nitroprusside caused significant shifts of erythrocytes microrheology, especially of erythrocytes aggregation. Sodium hydrosulfide moderately but statistically significant increased erythrocytes deformability and markedly reduced erythrocytes aggregation, but its effects were inferior to that of sodium nitroprusside. Conclusion. The study results suggest that guanylate cyclase and adenylate cyclase, as well as the ion channels of the cell membrane can be the intracellular signaling pathways in erythrocytes for investigated GTs.


Molecules ◽  
2021 ◽  
Vol 26 (15) ◽  
pp. 4533
Author(s):  
Ali Mohammad Pourbagher-Shahri ◽  
Tahereh Farkhondeh ◽  
Marjan Talebi ◽  
Dalia M. Kopustinskiene ◽  
Saeed Samarghandian ◽  
...  

Nitric Oxide (NO) is a potent signaling molecule involved in the regulation of various cellular mechanisms and pathways under normal and pathological conditions. NO production, its effects, and its efficacy, are extremely sensitive to aging-related changes in the cells. Herein, we review the mechanisms of NO signaling in the cardiovascular system, central nervous system (CNS), reproduction system, as well as its effects on skin, kidneys, thyroid, muscles, and on the immune system during aging. The aging-related decline in NO levels and bioavailability is also discussed in this review. The decreased NO production by endothelial nitric oxide synthase (eNOS) was revealed in the aged cardiovascular system. In the CNS, the decline of the neuronal (n)NOS production of NO was related to the impairment of memory, sleep, and cognition. NO played an important role in the aging of oocytes and aged-induced erectile dysfunction. Aging downregulated NO signaling pathways in endothelial cells resulting in skin, kidney, thyroid, and muscle disorders. Putative therapeutic agents (natural/synthetic) affecting NO signaling mechanisms in the aging process are discussed in the present study. In summary, all of the studies reviewed demonstrate that NO plays a crucial role in the cellular aging processes.


2018 ◽  
Vol 2018 ◽  
pp. 1-16 ◽  
Author(s):  
Dan Wu ◽  
Qingxun Hu ◽  
Deqiu Zhu

Hydrogen sulfide (H2S) and nitric oxide (NO) are now recognized as important regulators in the cardiovascular system, although they were historically considered as toxic gases. As gaseous transmitters, H2S and NO share a wide range of physical properties and physiological functions: they penetrate into the membrane freely; they are endogenously produced by special enzymes, they stimulate endothelial cell angiogenesis, they regulate vascular tone, they protect against heart injury, and they regulate target protein activity via posttranslational modification. Growing evidence has determined that these two gases are not independent regulators but have substantial overlapping pathophysiological functions and signaling transduction pathways. H2S and NO not only affect each other’s biosynthesis but also produce novel species through chemical interaction. They play a regulatory role in the cardiovascular system involving similar signaling mechanisms or molecular targets. However, the natural precise mechanism of the interactions between H2S and NO remains unclear. In this review, we discuss the current understanding of individual and interactive regulatory functions of H2S and NO in biosynthesis, angiogenesis, vascular one, cardioprotection, and posttranslational modification, indicating the importance of their cross-talk in the cardiovascular system.


Author(s):  
O. V. Bazilyuk ◽  
Anatolii V. Kotsuruba ◽  
Lyubov. G. Stepanenko ◽  
Sergey A. Talanov ◽  
Yu. P. Korchak ◽  
...  

2019 ◽  
Vol 72 (8) ◽  
pp. 1473-1476
Author(s):  
Nataliya Matolinets ◽  
Helen Sklyarova ◽  
Eugene Sklyarov ◽  
Andrii Netliukh

Introduction: Polytrauma patients have high risk of shock, septic complications and death during few years of follow-up. In recent years a lot of attention is paid to gaseous transmitters, among which are nitrogen oxide (NO) and hydrogen sulfide (H2S). It is known that the rise of NO and its metabolites levels occurs during the acute period of polytrauma. Nitric oxide and hydrogen sulfide are produced in different cell types, among which are lymphocytes. The aim: To investigate the levels of NO, NOS, iNOS, еNOS, H2S in lymphocytes lysate in patients at the moment of hospitalization and 24 hours after trauma. Materials and methods: We investigated the levels of NO, NO-synthase, inducible NO-synthase, endothelial NO-synthase, H2S in lymphocytes lysate in patients at the moment of hospitalization and 24 hours after trauma. Results: The study included 20 patients with polytrauma who were treated in the intensive care unit (ICU) of the Lviv Emergency Hospital. Tissue injury was associated with an increased production of NO, NOS, iNOS, еNOS during the acute period of polytrauma. At the same time, the level of H2S decreased by the end of the first day of traumatic injury. Conclusions: In acute period of polytrauma, significant increasing of iNOS and eNOS occurs with percentage prevalence of iNOS over eNOS on the background of H2S decreasing.


2018 ◽  
Vol 16 (2) ◽  
pp. 194-199
Author(s):  
Wioletta Ratajczak-Wrona ◽  
Ewa Jablonska

Background: Polymorphonuclear neutrophils (PMNs) play a crucial role in the innate immune system’s response to microbial pathogens through the release of reactive nitrogen species, including Nitric Oxide (NO). </P><P> Methods: In neutrophils, NO is produced by the inducible Nitric Oxide Synthase (iNOS), which is regulated by various signaling pathways and transcription factors. N-nitrosodimethylamine (NDMA), a potential human carcinogen, affects immune cells. NDMA plays a major part in the growing incidence of cancers. Thanks to the increasing knowledge on the toxicological role of NDMA, the environmental factors that condition the exposure to this compound, especially its precursors- nitrates arouse wide concern. Results: In this article, we present a detailed summary of the molecular mechanisms of NDMA’s effect on the iNOS-dependent NO production in human neutrophils. Conclusion: This research contributes to a more complete understanding of the mechanisms that explain the changes that occur during nonspecific cellular responses to NDMA toxicity.


2020 ◽  
Vol 16 ◽  
Author(s):  
Andrey Krylatov ◽  
Leonid Maslov ◽  
Sergey Y. Tsibulnikov ◽  
Nikita Voronkov ◽  
Alla Boshchenko ◽  
...  

: There is considerable evidence in the heart that autophagy in cardiomyocytes is activated by hypoxia/reoxygenation (H/R) or in hearts by ischemia/reperfusion (I/R). Depending upon the experimental model and duration of ischemia, increases in autophagy in this setting maybe beneficial (cardioprotective) or deleterious (exacerbate I/R injury). Aside from the conundrum as to whether or not autophagy is an adaptive process, it is clearly regulated by a number of diverse molecules including reactive oxygen species (ROS), various kinases, hydrogen sulfide (H2S) and nitric oxide (NO). The purpose this review is to address briefly the controversy regarding the role of autophagy in this setting and to examine a variety of disparate molecules that are involved in its regulation.


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