scholarly journals Physiology of Nitric Oxide in the Respiratory System

2017 ◽  
pp. S159-S172 ◽  
Author(s):  
M. ANTOSOVA ◽  
D. MOKRA ◽  
L. PEPUCHA ◽  
J. PLEVKOVA ◽  
T. BUDAY ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Lung Development ◽  
Clinical Manifestations ◽  
Physiological Role ◽  
No Production ◽  
Physiological Processes ◽  
Frequent Use ◽  
Organ Systems ◽  
Surfactant Production ◽  
And Function

Nitric oxide (NO) is an important endogenous neurotransmitter and mediator. It participates in regulation of physiological processes in different organ systems including airways. Therefore, it is important to clarify its role in the regulation of both airway and vascular smooth muscle, neurotransmission and neurotoxicity, mucus transport, lung development and in the surfactant production. The bioactivity of NO is highly variable and depends on many factors: the presence and activity of NO-producing enzymes, activity of competitive enzymes (e.g. arginase), the amount of substrate for the NO production, the presence of reactive oxygen species and others. All of these can change NO primary physiological role into potentially harmful. The borderline between them is very fragile and in many cases not entirely clear. For this reason, the research focuses on a comprehensive understanding of NO synthesis and its metabolic pathways, genetic polymorphisms of NO synthesizing enzymes and related effects. Research is also motivated by frequent use of exhaled NO monitoring in the clinical manifestations of respiratory diseases. The review focuses on the latest knowledge about the production and function of this mediator and understanding the basic physiological processes in the airways.

scholarly journals Smoking-Induced Inhibition of Number and Activity of Endothelial Progenitor Cells and Nitric Oxide in Males Were Reversed by Estradiol in Premenopausal Females

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Yijia Shao ◽  
Liang Luo ◽  
Zi Ren ◽  
Jiayi Guo ◽  
Xingxing Xiao ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cigarette Smoking ◽  
Premenopausal Women ◽  
Cross Sectional Study ◽  
Favorable Effect ◽  
No Production ◽  
Vascular Protection ◽  
Cross Sectional ◽  
And Function ◽  
Flow Mediated Vasodilation

Objectives. The number and activity of circulating EPCs were enhanced in premenopausal women contrast to postmenopausal females and age-matched males. Here, we investigated whether this favorable effect exists in premenopausal women and age-matched men with cigarette smoking. Methods. In a cross-sectional study, the number and activity of circulating EPCs and nitric oxide production (NO) as well as flow-mediated vasodilation (FMD) in both premenopausal women and age-matched men with or without cigarette smoking were studied. Results. Compared with age-matched men with or without smoking, the number and function of circulating EPCs as well as NO level in premenopausal women were obviously higher than that in the former and not affected by smoking. The number and function of circulating EPCs as well as NO level in male smokers were shown to be the most strongly inhibited. Furthermore, there was significant correlation between EPC number and activity, plasma NO level, and NO secretion by EPCs and FMD. Conclusions. Estradiol was deemed to play an important role in enhancing the number and activity of EPCs and NO production in premenopausal women even when affected by smoking, which may be the important mechanisms underlying vascular protection of estradiol in premenopausal women, but not in age-matched men.

Nitric oxide augments fetal pulmonary artery endothelial cell angiogenesis in vitro

2006 ◽  
Vol 290 (6) ◽  
pp. L1111-L1116 ◽  
Author(s):  
Vivek Balasubramaniam ◽  
Anne M. Maxey ◽  
Brian W. Fouty ◽  
Steven H. Abman
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cell ◽  
Oxygen Tension ◽  
Growth And Development ◽  
Tube Formation ◽  
No Production ◽  
Low Oxygen ◽  
Low Oxygen Tension ◽  
And Function ◽  
Pulmonary Artery Endothelial Cell

Growth and development of the lung normally occur in the low oxygen environment of the fetus. The role of this low oxygen environment on fetal lung endothelial cell growth and function is unknown. We hypothesized that low oxygen tension during fetal life enhances pulmonary artery endothelial cell (PAEC) growth and function and that nitric oxide (NO) production modulates fetal PAEC responses to low oxygen tension. To test this hypothesis, we compared the effects of fetal (3%) and room air (RA) oxygen tension on fetal PAEC growth, proliferation, tube formation, and migration in the presence and absence of the NO synthase (NOS) inhibitor Nω-nitro-l-arginine (LNA), and an NO donor, S-nitroso- N-acetylpenicillamine (SNAP). Compared with fetal PAEC grown in RA, 3% O2 increased tube formation by over twofold ( P < 0.01). LNA treatment reduced tube formation in 3% O2 but had no affect on tube formation in RA. Treatment with SNAP increased tube formation during RA exposure to levels observed in 3% O2. Exposure to 3% O2 for 48 h attenuated cell number (by 56%), and treatment with LNA reduced PAEC growth by 44% in both RA and 3% O2. We conclude that low oxygen tension enhances fetal PAEC tube formation and that NO is essential for normal PAEC growth, migration, and tube formation. Furthermore, we conclude that in fetal cells exposed to the relative hyperoxia of RA, 21% O2, NO overcomes the inhibitory effects of the increased oxygen, allowing normal PAEC angiogenesis and branching. We speculate that NO production maintains intrauterine lung vascular growth and development during exposure to low O2 in the normal fetus. We further speculate that NO is essential for pulmonary angiogenesis in fetal animal exposed to increased oxygen tension of RA and that impaired endothelial NO production may contribute to the abnormalities of angiogenesis see in infants with bronchopulmonary dysplasia.

New Strategy for Controlled Release of Nitric Oxide

2012 ◽  
Vol 20 ◽  
pp. 61-67 ◽  
Author(s):  
Amedea B. Seabra ◽  
Priscyla D. Marcato ◽  
Larissa B. de Paula ◽  
Nelson Durán
Keyword(s):  
Nitric Oxide ◽  
Vascular Tone ◽  
Polymeric Nanoparticles ◽  
No Production ◽  
Cell Replication ◽  
Neuronal Communication ◽  
Physiological Processes ◽  
Promising Strategy ◽  
New Strategy ◽  
Metal Organic

Nitric oxide (NO) is involved in several physiological processes, such as the control of vascular tone, the inhibition of platelet aggregation, smooth muscle cell replication, immune response and neuronal communication. Several pathologies have been associated to dysfunctions in the endogenous NO production. Thus, there is a great interest in the development of NO-releasing drugs and in matrices which are able to stabilize and release NO locally in different tissues. In this scenario, the preparation of NO-releasing nanomaterials, such as dendrimers, liposomes, metallic, silica, and polymeric nanoparticles, zeolites and metal organic frameworks, is a promising strategy for delivering NO in diverse applications, as discussed in this work.

scholarly journals Exogenous Nitro-Oleic Acid inhibits primary root growth by reducing the mitosis in the meristem in Arabidopsis thaliana

2020 ◽  
Author(s):  
Luciano M. Di Fino ◽  
Ignacio Cerrudo ◽  
Sonia R. Salvatore ◽  
Francisco J. Schopfer ◽  
Carlos García-Mata ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Fatty Acids ◽  
Oleic Acid ◽  
Root Growth ◽  
Unsaturated Fatty Acids ◽  
Primary Root ◽  
Cell Number ◽  
No Production ◽  
Physiological Processes ◽  
Primary Root Growth

ABSTRACTNitric oxide (NO) is a second messenger that regulates a broad range of physiological processes in plants. NO-derived molecules called reactive nitrogen species (RNS) can react with unsaturated fatty acids generating nitrated fatty acids (NO2-FA). NO2-FA work as signaling molecules in mammals where production and targets have been described under different stress conditions. Recently, NO2-FAs were detected in plants, however their role(s) on plant physiological processes is still poorly known. Here we show that exogenous application of nitro-oleic acid (NO2-OA) inhibits Arabidopsis primary root growth; this inhibition is not likely due to nitric oxide (NO) production or impaired auxin or cytokinin root responses. Deep analyses showed that roots incubated with NO2-OA had a lower cell number in the division area. Although this NO2-FA did not affect the signaling mechanisms maintaining the stem cell niche, plants incubated with NO2-OA showed a reduction of cell division in the meristematic area. Therefore, this work shows that NO2-OA inhibits mitotic processes subsequently reducing primary root growth.

scholarly journals Nitric Oxide-Mediated Posttranslational Modifications: Impacts at the Synapse

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Sophie A. Bradley ◽  
Joern R. Steinert
Keyword(s):  
Nitric Oxide ◽  
Synaptic Transmission ◽  
Posttranslational Modifications ◽  
Nitrosative Stress ◽  
Long Term Potentiation ◽  
No Production ◽  
Normal Brain ◽  
Calcium Dependent ◽  
Physiological Processes

Nitric oxide (NO) is an important gasotransmitter molecule that is involved in numerous physiological processes throughout the nervous system. In addition to its involvement in physiological plasticity processes (long-term potentiation, LTP; long-term depression, LTD) which can include NMDAR-mediated calcium-dependent activation of neuronal nitric oxide synthase (nNOS), new insights into physiological and pathological consequences of nitrergic signalling have recently emerged. In addition to the canonical cGMP-mediated signalling, NO is also implicated in numerous pathways involving posttranslational modifications. In this review we discuss the multiple effects of S-nitrosylation and 3-nitrotyrosination on proteins with potential modulation of function but limit the analyses to signalling involved in synaptic transmission and vesicular release. Here, crucial proteins which mediate synaptic transmission can undergo posttranslational modifications with either pre- or postsynaptic origin. During normal brain function, both pathways serve as important cellular signalling cascades that modulate a diverse array of physiological processes, including synaptic plasticity, transcriptional activity, and neuronal survival. In contrast, evidence suggests that aging and disease can induce nitrosative stressviaexcessive NO production. Consequently, uncontrolled S-nitrosylation/3-nitrotyrosination can occur and represent pathological features that contribute to the onset and progression of various neurodegenerative diseases, including Parkinson’s, Alzheimer’s, and Huntington’s.

scholarly journals Hypercapnia induces injury to alveolar epithelial cells via a nitric oxide-dependent pathway

2000 ◽  
Vol 279 (5) ◽  
pp. L994-L1002 ◽  
Author(s):  
John D. Lang ◽  
Phillip Chumley ◽  
Jason P. Eiserich ◽  
Alvaro Estevez ◽  
Thad Bamberg ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Epithelial Cells ◽  
Cell Injury ◽  
Inflammatory Responses ◽  
Alveolar Epithelial Cells ◽  
No Production ◽  
Inflammatory Reactions ◽  
Alveolar Epithelial ◽  
And Function ◽  
The Impact

Ventilator strategies allowing for increases in carbon dioxide (CO2) tensions (hypercapnia) are being emphasized to ameliorate the consequences of inflammatory-mediated lung injury. Inflammatory responses lead to the generation of reactive species including superoxide (O2 −), nitric oxide (·NO), and their product peroxynitrite (ONOO−). The reaction of CO2 and ONOO− can yield the nitrosoperoxocarbonate adduct ONOOCO2 −, a more potent nitrating species than ONOO−. Based on these premises, monolayers of fetal rat alveolar epithelial cells were utilized to investigate whether hypercapnia would modify pathways of ·NO production and reactivity that impact pulmonary metabolism and function. Stimulated cells exposed to 15% CO2 (hypercapnia) revealed a significant increase in ·NO production and nitric oxide synthase (NOS) activity. Cell 3-nitrotyrosine content as measured by both HPLC and immunofluorescence staining also increased when exposed to these same conditions. Hypercapnia significantly enhanced cell injury as evidenced by impairment of monolayer barrier function and increased induction of apoptosis. These results were attenuated by the NOS inhibitor N-monomethyl-l-arginine. Our studies reveal that hypercapnia modifies ·NO-dependent pathways to amplify cell injury. These results affirm the underlying role of ·NO in tissue inflammatory reactions and reveal the impact of hypercapnia on inflammatory reactions and its potential detrimental influences.

scholarly journals Morphofunctional platform for forming clinical symptoms of celiakia in children with connective tissue dysplasia

2021 ◽  
pp. 129-135
Author(s):  
Z. V. Nesterenko
Keyword(s):  
Celiac Disease ◽  
Connective Tissue ◽  
Clinical Manifestations ◽  
Structure And Function ◽  
Connective Tissue Disorders ◽  
Diverse Range ◽  
Organ Systems ◽  
And Function ◽  
The Impact

Review article on the problem of celiac disease, which is widespread with diverse range of clinical manifestations and inadequate diagnosis, is presented. The conciderable prevalence of connective tissue disorders in the pediatric population, the important role of connective tissue in the function of all organ systems, including the gastrointestinal system, necessitates studying the impact of the impaired structure and function of connective tissue on the development of celiac symptoms. The paper describes the historical development of the concept of “celiac disease”, the process of studying the pattern of the onset and development of symptoms of the disease; modern studies explaining the varied complex mechanisms of the disease.The article cites the researchers who studied the role of connective tissue in the structure and function of all body systems with identifying the impact of connective tissue disorders on the development of the gastrointestinal pathology (abnormal motor- tonic activity, reflux disease, dysbiosis, disturbance of autonomic homeostasis) and the manifestation of celiac disease associated with connective tissue disorders.The conclusion stresses the need to consider the problem of celiac disease as a manifestation of the pathology of the whole organism with the obligatory diagnosis of comorbid diseases, including those associated with connective tissue disorders, which will provide a more successful therapy for celiac disease and an improved prognosis.

scholarly journals Glycyrrhizin as a Nitric Oxide Regulator in Cancer Chemotherapy

Cancers ◽  
2021 ◽  
Vol 13 (22) ◽  
pp. 5762
Author(s):  
Minsu Kim ◽  
Seok Chan Park ◽  
Dong Yun Lee
Keyword(s):  
Nitric Oxide ◽  
Multidrug Resistance ◽  
Tumor Microenvironment ◽  
Cancer Chemotherapy ◽  
Active Compound ◽  
Potential Role ◽  
No Production ◽  
Therapeutic Benefits ◽  
And Function

Chemotherapy is used widely for cancer treatment; however, the evolution of multidrug resistance (MDR) in many patients limits the therapeutic benefits of chemotherapy. It is important to overcome MDR for enhanced chemotherapy. ATP-dependent efflux of drugs out of cells is the main mechanism of MDR. Recent studies have suggested that nitric oxide (NO) can be used to overcome MDR by inhibiting the ATPase function of ATP-dependent pumps. Several attempts have been made to deliver NO to the tumor microenvironment (TME), however there are limitations in delivery. Glycyrrhizin (GL), an active compound of licorice, has been reported to both reduce the MDR effect by inhibiting ATP-dependent pumps and function as a regulator of NO production in the TME. In this review, we describe the potential role of GL as an NO regulator and MDR inhibitor that efficiently reduces the MDR effect in cancer chemotherapy.

scholarly journals Atg32 dependent mitophagy sustains spermidine and nitric oxide required for heat stress tolerance in S. cerevisiae

2021 ◽  
Author(s):  
Jasvinder Kaur ◽  
Juliet Goldsmith ◽  
Alexandra Tankka ◽  
Sofía Bustamante Eguiguren ◽  
Alfredo A. Gimenez ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heat Stress ◽  
Molecular Mechanisms ◽  
Physiological Role ◽  
No Production ◽  
Polyamine Biosynthesis ◽  
Adenosyl Methionine ◽  
Autophagic Degradation ◽  
Respiratory Growth ◽  
Induced Defects

In Saccharomyces cerevisiae, the selective autophagic degradation of mitochondria, termed mitophagy, is critically regulated by the adapter protein, Atg32. Despite our knowledge about the molecular mechanisms by which Atg32 controls mitophagy, its physiological roles in yeast survival and fitness remains less clear. Here, we demonstrate a requirement for Atg32 in promoting spermidine production during respiratory growth and heat-induced mitochondrial stress. During respiratory growth, mitophagy-deficient yeast exhibit profound heat-stress induced defects in growth and viability due to impaired biosynthesis of spermidine and its biosynthetic precursor S-Adenosyl-Methionine (SAM). Moreover, spermidine production is crucial for the induction of cytoprotective nitric oxide (NO) during heat stress. Hence, the re-addition of spermidine to Atg32 mutant yeast is sufficient to both enhance NO production and restore respiratory growth during heat stress. Our findings uncover a previously unrecognized physiological role for yeast mitophagy in spermidine metabolism and illuminate new interconnections between mitophagy, polyamine biosynthesis and NO signaling.

scholarly journals Peroxynitrites and impaired modulation of nitric oxide concentrations in embryos from diabetic rats during early organogenesis

Reproduction ◽  
2005 ◽  
Vol 130 (5) ◽  
pp. 695-703 ◽  
Author(s):  
A Jawerbaum ◽  
R Higa ◽  
V White ◽  
E Capobianco ◽  
C Pustovrh ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitrosative Stress ◽  
Maternal Diabetes ◽  
Inhibitory Effect ◽  
Signaling Molecules ◽  
Diabetic Rats ◽  
Prostaglandin E ◽  
No Production ◽  
Diabetic Embryopathy ◽  
And Function

Maternal diabetes significantly increases the risk of congenital malformation, a syndrome known as diabetic embryopathy. Nitric oxide (NO), implicated in embryogenesis, has been found elevated in embryos from diabetic rats during organogenesis. The developmental signaling molecules endothelin-1 (ET-1) and 15-deoxy Δ12,14prostaglandin J2 (15dPGJ2) downregulate embryonic NO levels. In the presence of NO and superoxide, formation of the potent oxidant peroxynitrite may occur. Therefore, we investigated peroxynitrite-induced damage, ET-1 and 15dPGJ2 concentrations, and the capability of ET-1, 15dPGJ2 and prostaglandin E2 (PGE2) to regulate NO production in embryos from severely diabetic rats (streptozotocin-induced before pregnancy). We found intense nitrotyrosine immunostaining (an index of peroxynitrite-induced damage) in neural folds, neural tube and developing heart of embryos from diabetic rats (P < 0.001 vs controls). We also found reduced ET-1 (P < 0.001) and 15dPGJ2 (P < 0.001) concentrations in embryos from diabetic rats when compared with controls. In addition, the inhibitory effect of ET-1, 15dPGJ2 and PGE2 on NO production found in control embryos was not observed in embryos from severely diabetic rats. In conclusion, both the demonstrated peroxynitrite-induced damage and the altered levels and function of multiple signaling molecules involved in the regulation of NO production provide supportive evidence of nitrosative stress in diabetic embryopathy.

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