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Journal articles on the topic 'Nitric oxide bioavailability'

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Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

Sobolewski, Peter, Irene Gramaglia, John Frangos, Marcos Intaglietta, and Henri C. van der Heyde. "Nitric oxide bioavailability in malaria." Trends in Parasitology 21, no. 9 (September 2005): 415–22. http://dx.doi.org/10.1016/j.pt.2005.07.002.

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2

HEYMAN, SAMUEL N., MARINA GOLDFARB, DAVID DARMON, and MAYER BREZIS. "Tissue Oxygenation Modifies Nitric Oxide Bioavailability." Microcirculation 6, no. 3 (September 1999): 199–203. http://dx.doi.org/10.1111/j.1549-8719.1999.tb00102.x.

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3

Suschek, Christoph V., Dennis Feibel, Maria von Kohout, and Christian Opländer. "Enhancement of Nitric Oxide Bioavailability by Modulation of Cutaneous Nitric Oxide Stores." Biomedicines 10, no. 9 (August 29, 2022): 2124. http://dx.doi.org/10.3390/biomedicines10092124.

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The generation of nitric oxide (NO) in the skin plays a critical role in wound healing and the response to several stimuli, such as UV exposure, heat, infection, and inflammation. Furthermore, in the human body, NO is involved in vascular homeostasis and the regulation of blood pressure. Physiologically, a family of enzymes termed nitric oxide synthases (NOS) generates NO. In addition, there are many methods of non-enzymatic/NOS-independent NO generation, e.g., the reduction of NO derivates (NODs) such as nitrite, nitrate, and nitrosylated proteins under certain conditions. The skin is the largest and heaviest human organ and contains a comparatively high concentration of these NODs; therefore, it represents a promising target for many therapeutic strategies for NO-dependent pathological conditions. In this review, we give an overview of how the cutaneous NOD stores can be targeted and modulated, leading to a further accumulation of NO-related compounds and/or the local and systemic release of bioactive NO, and eventually, NO-related physiological effects with a potential therapeutical use for diseases such as hypertension, disturbed microcirculation, impaired wound healing, and skin infections.

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4

&NA;. "Clopidogrel improves nitric oxide bioavailability in CAD." Inpharma Weekly &NA;, no. 1550 (August 2006): 19. http://dx.doi.org/10.2165/00128413-200615500-00050.

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5

Price, Daniel T., Joseph A. Vita, and John F. Keaney. "Redox Control of Vascular Nitric Oxide Bioavailability." Antioxidants & Redox Signaling 2, no. 4 (December 2000): 919–35. http://dx.doi.org/10.1089/ars.2000.2.4-919.

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6

Huang, K. T., T. H. Han, D. R. Hyduke, M. W. Vaughn, H. Van Herle, T. W. Hein, C. Zhang, L. Kuo, and J. C. Liao. "Modulation of nitric oxide bioavailability by erythrocytes." Proceedings of the National Academy of Sciences 98, no. 20 (September 25, 2001): 11771–76. http://dx.doi.org/10.1073/pnas.201276698.

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7

Chen, Jing-yi, Zi-xin Ye, Xiu-fen Wang, Jian Chang, Mei-wen Yang, Hua-hua Zhong, Fen-fang Hong, and Shu-long Yang. "Nitric oxide bioavailability dysfunction involves in atherosclerosis." Biomedicine & Pharmacotherapy 97 (January 2018): 423–28. http://dx.doi.org/10.1016/j.biopha.2017.10.122.

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8

Lai, Wai Keung Christopher, and Ming Yin Kan. "Homocysteine-Induced Endothelial Dysfunction." Annals of Nutrition and Metabolism 67, no. 1 (2015): 1–12. http://dx.doi.org/10.1159/000437098.

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This review discussed and in particular emphasis the potential cellular pathways and the biological processes involved that lead to homocysteine-induced endothelial dysfunction, in particular in the impaired endothelial dependent dilatation aspect. Hyperhomocysteinemia is an independent cardiovascular risk factor that has been associated with atherosclerotic vascular diseases and ischemic heart attacks. The potential mechanisms by which elevated plasma homocysteine level leads to reduction in nitric oxide bioavailability include the disruptive uncoupling of nitric oxide synthase activity and quenching of nitric oxide by oxidative stress, the enzymatic inhibition by asymmetric dimethylarginine, endoplasmic reticulum stress with eventual endothelial cell apoptosis, and chronic inflammation/prothrombotic conditions. Homocysteine-induced endothelial dysfunction presumably affecting the bioavailability of the potent vasodilator ‘nitric oxide', and such dysfunction can easily be monitor by flow-mediated dilation method using ultrasound. Understanding the mechanisms by which plasma homocysteine alter endothelial nitric oxide production is therefore essential in the comprehension of homocysteine-induced impairment of endothelial dependent dilatation, and its association of cardiovascular risk and its pathophysiology.

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9

Liu, Xiaoyu, John Fassett, Yidong Wei, and Yingjie Chen. "Regulation of DDAH1 as a Potential Therapeutic Target for Treating Cardiovascular Diseases." Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–6. http://dx.doi.org/10.1155/2013/619207.

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Asymmetric dimethylarginine (ADMA) is an endogenous nitric oxide synthase inhibitor that blocks nitric oxide production, while congestive heart failure is associated with increased plasma and tissue ADMA content. Increased plasma ADMA is a strong and independent predictor of all-cause mortality in the community and the strongest predictor of mortality in patients after myocardial infarction. Recent studies demonstrated that dimethylarginine dimethylaminohydrolase-1 (DDAH1) is the critical enzyme for ADMA degradation and thereby plays an important role in maintaining cardiovascular nitric oxide bioavailability. Interestingly, activation of the farnesoid X receptor (FXR) through the bile acid ursodeoxycholic acid (UDCA) or synthetic FXR agonists, such as GW4064, can increase DDAH1 expression. Thus, modulating DDAH1 activity through FXR receptor agonists such as UDCA could be a therapeutic target for treating reduced nitric oxide bioavailability in congestive heart failure and other cardiovascular diseases.

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10

Rush, James W. E., Steven G. Denniss, and Drew A. Graham. "Vascular Nitric Oxide and Oxidative Stress: Determinants of Endothelial Adaptations to Cardiovascular Disease and to Physical Activity." Canadian Journal of Applied Physiology 30, no. 4 (August 1, 2005): 442–74. http://dx.doi.org/10.1139/h05-133.

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Cardiovascular disease is the single leading cause of death and morbidity for Canadians. A universal feature of cardiovascular disease is dysfunction of the vascular endothelium, thus disrupting control of vasodilation, tissue perfusion, hemostasis, and thrombosis. Nitric oxide bioavailability, crucial for maintaining vascular endothelial health and function, depends on the processes controlling synthesis and destruction of nitric oxide as well as on the sensitivity of target tissue to nitric oxide. Evidence supports a major contribution by oxidative stress-induced destruction of nitric oxide to the endothelial dysfunction that accompanies a number of cardiovascular disease states including hypertension, diabetes, chronic heart failure, and atherosclerosis. Regular physical activity (exercise training) reduces cardiovascular disease risk. Numerous studies support the hypothesis that exercise training improves vascular endothelial function, especially when it has been impaired by preexisting risk factors. Evidence is emerging to support a role for improved nitric oxide bioavailability with training as a result of enhanced synthesis and reduced oxidative stress-mediated destruction. Molecular targets sensitive to the exercise training effect include the endothelial nitric oxide synthase and the antioxidant enzyme superoxide dismutase. However, many fundamental details of the cellular and molecular mechanisms linking exercise to altered molecular and functional endothelial phenotypes have yet to be discovered. The working hypothesis is that some of the cellular mechanisms contributing to endothelial dysfunction in cardiovascular disease can be targeted and reversed by signals associated with regular increases in physical activity. The capacity for exercise training to regulate vascular endothelial function, nitric oxide bioavailability, and oxidative stress is an example of how lifestyle can complement medicine and pharmacology in the prevention and management of cardiovascular disease. Key words: exercise, artery, reactive oxygen species, antioxidant, hypertension

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11

Delgado, María Gabriela, Jordi Gracia-Sancho, Giusi Marrone, Aina Rodríguez-Vilarrupla, Ramon Deulofeu, Juan G. Abraldes, Jaume Bosch, and Juan Carlos García-Pagán. "Leptin receptor blockade reduces intrahepatic vascular resistance and portal pressure in an experimental model of rat liver cirrhosis." American Journal of Physiology-Gastrointestinal and Liver Physiology 305, no. 7 (October 1, 2013): G496—G502. http://dx.doi.org/10.1152/ajpgi.00336.2012.

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Increased hepatic vascular resistance mainly due to elevated vascular tone and to fibrosis is the primary factor in the development of portal hypertension in cirrhosis. Leptin, a hormone associated with reduction in nitric oxide bioavailability, vascular dysfunction, and liver fibrosis, is increased in patients with cirrhosis. We aimed at evaluating whether leptin influences the increased hepatic resistance in portal hypertension. CCl4-cirrhotic rats received the leptin receptor-blocker ObR antibody, or its vehicle, every other day for 1 wk. Hepatic and systemic hemodynamics were measured in both groups. Hepatic nitric oxide production and bioavailability, together with oxidative stress, nitrotyrosinated proteins, and liver fibrosis, were evaluated. In cirrhotic rats, leptin-receptor blockade significantly reduced portal pressure without modifying portal blood flow, suggesting a reduction in the intrahepatic resistance. Portal pressure reduction was associated with increased nitric oxide bioavailability and with decreased O2− levels and nitrotyrosinated proteins. No changes in systemic hemodynamics and liver fibrosis were observed. In conclusion, the present study shows that blockade of the leptin signaling pathway in cirrhosis significantly reduces portal pressure. This effect is probably due to a nitric oxide-mediated reduction in the hepatic vascular tone.

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12

Sertório, J. T., R. Lacchini, L. M. Amaral, A. C. T. Palei, R. C. Cavalli, V. C. Sandrim, G. Duarte, and J. E. Tanus-Santos. "Haptoglobin polymorphism affects nitric oxide bioavailability in preeclampsia." Journal of Human Hypertension 27, no. 6 (December 6, 2012): 349–54. http://dx.doi.org/10.1038/jhh.2012.57.

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13

Jeffers, Anne B., and Daniel B. Kim-Shapiro. "P031. Effects of hemolysis on nitric oxide bioavailability." Nitric Oxide 14, no. 4 (June 2006): 28. http://dx.doi.org/10.1016/j.niox.2006.04.092.

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14

Andreotti, Felicita, Teodosio Pafundi, Giulio Coluzzi, and Attilio Maseri. "Hemoglobin Levels, Nitric Oxide Bioavailability and Cardiovascular Outcomes." American Journal of Cardiology 107, no. 7 (April 2011): 1099. http://dx.doi.org/10.1016/j.amjcard.2010.12.028.

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15

Verma, Subodh, and Milan K. Gupta. "Aliskiren Improves Nitric Oxide Bioavailability and Limits Atherosclerosis." Hypertension 52, no. 3 (September 2008): 467–69. http://dx.doi.org/10.1161/hypertensionaha.108.114488.

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16

Mitchell, Brett M., and R. Clinton Webb. "Impaired Vasodilation and Nitric Oxide Synthase Activity in Glucocorticoid-Induced Hypertension." Biological Research For Nursing 4, no. 1 (July 2002): 16–21. http://dx.doi.org/10.1177/1099800402004001003.

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Synthetic glucocorticoids are among the most widely prescribed medications by physicians. Although they have a vast array of beneficial effects such as immunosuppression and anti-inflammation, excess glucocorticoids can lead to iatrogenic Cushing’s syndrome, which includes hypertension and cardiovascular disease. The exact mechanism by which glucocorticoids elevate blood pressure is not completely understood, but it appears to be a complex pathology that involves increased responsiveness to vasoconstrictors and decreased vasodilator production. Nitric oxide is a vasodilator that plays a key role in blood pressure regulation, and previous studies have shown that a reduction in nitric oxide production or bioavailability contributes to hypertension. Tetrahydrobiopterin, a necessary cofactor for nitric oxide synthase activity, can affect nitric oxide production and bioavailability, with low levels causing decreased nitric oxide production. However, little is known about the interaction between glucocorticoids and tetrahydrobiopterin levels. In this review, the roles of nitric oxide and tetrahydrobiopterin in the pathogenesis of glucocorticoid hypertension will be discussed. Furthermore, the authors propose that glucocorticoids exert a genomic effect to decrease guanosine triphosphate cyclohydrolase I, the rate-limiting enzyme in the production of tetrahydrobiopterin. In the future, tetrahydrobiopterin supplementation in patients with iatrogenic Cushing’s syndrome may prove to be beneficial and decrease mortality attributed to cardiovascular disease.

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17

Schenkel, Paulo C., Rafael O. Fernandes, Vinícius U. Viegas, Cristina Campos, Tânia R. G. Fernandes, Alex Sander da Rosa Araujo, and Adriane Belló-Klein. "Catalase Influence in the Regulation of Coronary Resistance by Estrogen: Joint Action of Nitric Oxide and Hydrogen Peroxide." Oxidative Medicine and Cellular Longevity 2014 (2014): 1–6. http://dx.doi.org/10.1155/2014/159852.

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We tested the influence of estrogen on coronary resistance regulation by modulating nitric oxide (NO) and hydrogen peroxide (H2O2) levels in female rats. For this, estrogen levels were manipulated and the hearts were immediately excised and perfused at a constant flow using a Langendorff’s apparatus. Higher estrogen levels were associated with a lower coronary resistance, increased nitric oxide bioavailability, and higher levels of H2O2. When oxide nitric synthase blockade by L-NAME was performed, no significant changes were found in coronary resistance of ovariectomized rats. Additionally, we found an inverse association between NO levels and catalase activity. Taken together, our data suggest that, in the absence of estrogen influence and, therefore, reduced NO bioavailability, coronary resistance regulation seems to be more dependent on the H2O2that is maintained at low levels by increased catalase activity.

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18

Garalienė, Vida. "Endothelium and nitric oxide." Medicina 44, no. 7 (June 30, 2008): 564. http://dx.doi.org/10.3390/medicina44070073.

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Studied nature of the “blood vessels relaxing factor” derived fromendotheliumthat was identified as nitric oxide caused intensive scientific research on nitric oxide regarding some aspects of its impact on human physiological and pathological processes. The objective of this short review is to discuss widely used (in the clinical practice) direct and indirect donors of nitric oxide and/or other agents, increasing nitric oxide concentration in human body, and their beneficial role for the prevention of atherosclerosis. Under physiological conditions, endotheliumregulates the tone of blood vessels, homeostasis of which is maintained by endotheliumgenerated vasoconstrictors and vasodilators. The most important vasodilator and the main substance produced by the endothelium is nitric oxide. The failure of synthesis and/or the lost of nitric oxide bioavailability is the major feature of endothelial dysfunction and key factor initiating progression of atherosclerosis. The endothelial dysfunction initiates the series of events, which stimulate and aggravate the course of atherosclerosis by increasing endothelial permeability, platelet aggregation, and leukocyte adhesion, and cytokine expression. Further, the review deals with the mechanisms of action of statins, angiotensin-converting enzyme inhibitors, L-arginine, direct nitric oxide donors (nitroglycerin, isosorbide mononitrate and isosorbide dinitrate), and indirect nitric oxide donors (phosphodiesterase-V inhibitors, KATP openers).

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19

Grasemann, Hartmut, Rupinder Dhaliwal, Julijana Ivanovska, Crystal Kantores, Patrick J. McNamara, Jeremy A. Scott, Jaques Belik, and Robert P. Jankov. "Arginase inhibition prevents bleomycin-induced pulmonary hypertension, vascular remodeling, and collagen deposition in neonatal rat lungs." American Journal of Physiology-Lung Cellular and Molecular Physiology 308, no. 6 (March 15, 2015): L503—L510. http://dx.doi.org/10.1152/ajplung.00328.2014.

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Arginase is an enzyme that limits substrate l-arginine bioavailability for the production of nitric oxide by the nitric oxide synthases and produces l-ornithine, which is a precursor for collagen formation and tissue remodeling. We studied the pulmonary vascular effects of arginase inhibition in an established model of repeated systemic bleomycin sulfate administration in neonatal rats that results in pulmonary hypertension and lung injury mimicking the characteristics typical of bronchopulmonary dysplasia. We report that arginase expression is increased in the lungs of bleomycin-exposed neonatal rats and that treatment with the arginase inhibitor amino-2-borono-6-hexanoic acid prevented the bleomycin-induced development of pulmonary hypertension and deposition of collagen. Arginase inhibition resulted in increased l-arginine and l-arginine bioavailability and increased pulmonary nitric oxide production. Arginase inhibition also normalized the expression of inducible nitric oxide synthase, and reduced bleomycin-induced nitrative stress while having no effect on bleomycin-induced inflammation. Our data suggest that arginase is a promising target for therapeutic interventions in neonates aimed at preventing lung vascular remodeling and pulmonary hypertension.

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20

Muller-Delp, J. M. "Ascorbic acid and tetrahydrobiopterin: looking beyond nitric oxide bioavailability." Cardiovascular Research 84, no. 2 (September 10, 2009): 178–79. http://dx.doi.org/10.1093/cvr/cvp307.

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21

Bolden, Crystal, Casey Schuck, S. Bruce King, and Daniel Kim-Shapiro. "Exploring the effect of sulfide on nitric oxide bioavailability." Nitric Oxide 42 (November 2014): 106. http://dx.doi.org/10.1016/j.niox.2014.09.025.

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22

Jeffers, Anne, Mark Gladwin, and Daniel Kim-Shapiro. "Computational Modeling of Nitric Oxide Bioavailability in Hemolytic Anemias." Blood 108, no. 11 (November 16, 2006): 1209. http://dx.doi.org/10.1182/blood.v108.11.1209.1209.

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Abstract Intravascular hemoglobin (Hb) scavenges nitric oxide (NO), which decreases the availability of endothelial-derived NO, thereby reducing smooth muscle relaxation. Under normal conditions, there are various mechanisms that limit consumption of NO by Hb in vivo includinga physical barrier to NO diffusion across the red blood cell (RBC) membrane,an unstirred layer creating a concentration gradient in NO outside the RBC, andand a cell-free zone between the endothelium where NO is made and the location of the RBCs. However, in hemolytic conditions, these mechanisms can be compromised, leading to reduced levels of NO reaching the smooth muscle cells to cause vasodilation. Although it is generally accepted that cell-free Hb scavenges NO more effectively than Hb encapsulated in the red blood cell (RBC), some do not believe that the low concentrations of cell-free Hb that are present in hemolytic conditions, such as sickle cell disease, can impact NO bioavailability in the presence of the large amounts of RBC encapsulated Hb (about 10 mM in heme) present in vivo. We have performed computational modeling looking at the effects of cell-free Hb on NO bioavailability within blood vessels. We have found that concentrations of cell-free Hb as low as one micromolar significantly reduces the availability of NO. Thus, 0.01% hemolysis has a significant affect on steady state NO levels. Extravasation of cell-free Hb into the interstitial space of as low as one micromolar further reduces the bioavailability of NO. At low hematocrit values, cell-free Hb scavenging of NO was found to be more efficient than at high hematocrit values. We have also found that the effect of RBC membrane permeability diminishes at cell-free Hb concentrations of only four micromolar and above. These theoretical results support experimental evidence indicating that cell-free Hb contributes to the pathology of hemolytic diseases. Supported by NIH grant RG0489.

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23

Berkels, Reinhard, Guido Egink, Tobias A. Marsen, Henning Bartels, Renate Roesen, and Wolfgang Klaus. "Nifedipine Increases Endothelial Nitric Oxide Bioavailability by Antioxidative Mechanisms." Hypertension 37, no. 2 (February 2001): 240–45. http://dx.doi.org/10.1161/01.hyp.37.2.240.

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24

Prasad, Abhiram, Neil P. Andrews, Feroz A. Padder, Mohsin Husain, and Arshed A. Quyyumi. "Glutathione reverses endothelial dysfunction and improves nitric oxide bioavailability." Journal of the American College of Cardiology 34, no. 2 (August 1999): 507–14. http://dx.doi.org/10.1016/s0735-1097(99)00216-8.

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25

Gruber, H.-J., C. Mayer, H. Mangge, G. Fauler, N. Grandits, and M. Wilders-Truschnig. "Obesity reduces the bioavailability of nitric oxide in juveniles." International Journal of Obesity 32, no. 5 (January 15, 2008): 826–31. http://dx.doi.org/10.1038/sj.ijo.0803795.

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26

Venardos, Kylie M., Laura Willems, and David M. Kaye. "Augmenting Nitric Oxide (NO) Bioavailability Reduces Ischaemic Myocardial Injury." Heart, Lung and Circulation 16 (January 2007): S28. http://dx.doi.org/10.1016/j.hlc.2007.06.073.

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27

Gajecki, Damian, Jakub Gawryś, Jerzy Wiśniewski, Paulina Fortuna, Ewa Szahidewicz-Krupska, and Adrian Doroszko. "A Cross-Talk between the Erythrocyte L-Arginine/ADMA/Nitric Oxide Metabolic Pathway and the Endothelial Function in Subjects with Type 2 Diabetes Mellitus." Nutrients 13, no. 7 (July 4, 2021): 2306. http://dx.doi.org/10.3390/nu13072306.

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(1) Background: Type-2-diabetes-mellitus (DM) is one the most important cardiovascular-risk-factors. Among many molecules regulating vascular tone, nitric oxide appears to be the most pivotal. Although micro- and macrovascular-abnormalities are extensively studied, the alterations in the nitric-oxide-metabolic-pathway require further investigations. Additionally, the role of erythrocytes in the vascular tone regulation has not been extensively explored. The aim of this study was to evaluate the endothelial-function and the nitric-oxide-metabolic-pathway in erythrocytes and plasma of diabetic individuals. (2) Methods: A total of 80 subjects were enrolled in this cross-sectional study, including 35 patients with DM and 45 healthy individuals. The endothelial-function was evaluated in response to different stimuli. (3) Results: In the DM group, decreased Arginine and citrulline concentrations in the plasma compartment with reduced Arginine/ADMA and ADMA/DMA-ratios were observed. Preserved nitric-oxide-metabolism in erythrocytes with reduced citrulline level and significantly higher NO-bioavailability were noted. Significant endothelial dysfunction in DM individuals was proved in response to the heat-stimulus. (4) Conclusions: DM patients at an early stage of disease show significant differences in the nitric-oxide-metabolic-pathway, which are more pronounced in the plasma compartment. Erythrocytes constitute a buffer with a higher nitric-oxide-bioavailability, less affected by the DM-related deviations. Patients at an early-stage of DM reveal endothelial-dysfunction, which could be diagnosed earlier using the laser-Doppler-flowmetry.

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28

Orenha, Renato Pereira, Graziele Cappato Guerra Silva, Ana Paula de Lima Batista, Antonio Gustavo Sampaio de Oliveira Filho, Nelson Henrique Morgon, Vanessa Borges da Silva, Saulo Samuel Pereira Furtado, Giovanni Finoto Caramori, Maurício Jeomar Piotrowski, and Renato Luis Tame Parreira. "Tracking the role of trans-ligands in ruthenium–NO bond lability: computational insight." New Journal of Chemistry 44, no. 27 (2020): 11448–56. http://dx.doi.org/10.1039/d0nj01340d.

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29

Pinheiro, Andressa Kely, Dalila Andrade Pereira, Jean Leandro dos Santos, Fabiano Beraldi Calmasini, Eduardo Costa Alexandre, Leonardo Oliveira Reis, Arthur L. Burnett, Fernando Ferreira Costa, and Fábio Henrique Silva. "Resveratrol-nitric oxide donor hybrid effect on priapism in sickle cell and nitric oxide-deficient mouse." PLOS ONE 17, no. 6 (June 2, 2022): e0269310. http://dx.doi.org/10.1371/journal.pone.0269310.

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Background Children and adult with sickle cell disease (SCD) display priapism associated with low nitric oxide (NO) bioavailability and oxidative stress in penis. Aim This study aimed to evaluate the effects of hybrid compound RVT-FxMe, derived from resveratrol bearing a NO-donor subunit, on two murine model that display priapism phenotype, SCD transgenic mice and endothelial NO synthase gene-deficient (eNOS-/-) mice. Methods Wild-type, SCD, and eNOS-/- mice were treated with RVT-FxMe (25 mg/kg/d, 2 weeks). Outcomes Hematological parameters, concentration-response curves to acetylcholine (ACh) and sodium nitroprusside (SNP), as well as to electrical field stimulation (EFS), were obtained in mice corpus cavernosum strips. Results Corpus cavernosum relaxations to SNP and EFS were increased in eNOS-/- group, which were normalized by RVT-FxMe treatment. SCD mice exhibited an excessive CC relaxant response induced by ACh, EFS and SNP RVT-FxMe treatment did not change the increased relaxant responses to ACh, EFS and SNP in corpus cavernosum from SCD group. Clinical translation Excess of plasma hemoglobin in SCD may interfere in pharmacological activity of NO donors compounds. Strength/Limitations While mechanistic data with promising potential is showed, the current study is not without limitations. RVT-FxMe effects in the mid- and long-term warrant complementary studies. Conclusion Treatment with RVT-FxMe reversed the enhanced NO-cGMP-mediated CC relaxations in eNOS-/- mice, but not in SCD mice; it is likely that excess of plasma hemoglobin in SCD mice act to inactivate NO before it reaches soluble guanylyl cyclase, avoiding restoration of NO bioavailability in penis.

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30

Taylor, Crystal M., Malgorzata Kasztan, Randee Sedaka, Patrick A. Molina, Luke S. Dunaway, Jennifer S. Pollock, and David M. Pollock. "Hydroxyurea improves nitric oxide bioavailability in humanized sickle cell mice." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 320, no. 5 (May 1, 2021): R630—R640. http://dx.doi.org/10.1152/ajpregu.00205.2020.

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Despite advancements in disease management, sickle cell nephropathy, a major contributor to mortality and morbidity in patients, has limited therapeutic options. Previous studies indicate hydroxyurea, a commonly prescribed therapy for sickle cell disease (SCD), can reduce renal injury in SCD but the mechanisms are uncertain. Because SCD is associated with reduced nitric oxide (NO) bioavailability, we hypothesized that hydroxyurea treatment would improve NO bioavailability in the humanized sickle cell mouse. Humanized male 12-wk-old sickle (HbSS) and genetic control (HbAA) mice were treated with hydroxyurea or regular tap water for 2 wk before renal and systemic NO bioavailability as well as renal injury were assessed. Untreated HbSS mice exhibited increased proteinuria, elevated plasma endothelin-1 (ET-1), and reduced urine concentrating ability compared with HbAA mice. Hydroxyurea reduced proteinuria and plasma ET-1 levels in HbSS mice. Untreated HbSS mice had reduced plasma nitrite and elevated plasma arginase concentrations compared with HbAA mice. Hydroxyurea treatment augmented plasma nitrite and attenuated plasma arginase in HbSS mice. Renal vessels isolated from HbSS mice also had elevated nitric oxide synthase 3 (NOS3) and arginase 2 expression compared with untreated HbAA mice. Hydroxyurea treatment did not alter renal vascular NOS3, however, renal vascular arginase 2 expression was significantly reduced. These data support the hypothesis that hydroxyurea treatment augments renal and systemic NO bioavailability by reducing arginase activity as a potential mechanism for the improvement on renal injury seen in SCD mice.

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31

Hyndman, Mathew Eric, Subodh Verma, Robin J. Rosenfeld, Todd J. Anderson, and Howard G. Parsons. "Interaction of 5-methyltetrahydrofolate and tetrahydrobiopterin on endothelial function." American Journal of Physiology-Heart and Circulatory Physiology 282, no. 6 (June 1, 2002): H2167—H2172. http://dx.doi.org/10.1152/ajpheart.00935.2001.

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The present study was designed to investigate the interaction between 5-methyltetrahydrofolate and tetrahydrobiopterin in modulating endothelial function. Tetrahydrobiopterin is a critical cofactor for nitric oxide synthase and maintains this enzyme as a nitric oxide- versus superoxide-producing enzyme. The structure of 5-methyltetrahydrofolate is similar to tetrahydrobiopterin and both agents have been shown to improve endothelium-dependent vasodilatation. We hypothesized that 5-methyltetrahydrofolate interacts with nitric oxide synthase in a fashion analogous, yet independent, of tetrahydrobiopterin to improve endothelial function. We demonstrate that 5-methyltetrahydrofolate binds the active site of nitric oxide synthase and mimics the orientation of tetrahydrobiopterin. Furthermore, 5-methyltetrahydrofolate attenuates superoxide production (induced by inhibition of tetrahydrobiopterin synthesis) and improves endothelial function in aortae isolated from tetrahydrobiopterin-deficient rats. We suggest that 5-methyltetrahydrofolate directly interacts with nitric oxide synthase to promote nitric oxide (vs. superoxide) production and improve endothelial function. 5-Methyltetrahydrofolate may represent an important strategy for intervention aimed at improving tetrahydrobiopterin bioavailability.

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32

Brodsky, Sergey V., Albert Marcus Morrishow, Nimish Dharia, Steven S. Gross, and Michael S. Goligorsky. "Glucose scavenging of nitric oxide." American Journal of Physiology-Renal Physiology 280, no. 3 (March 1, 2001): F480—F486. http://dx.doi.org/10.1152/ajprenal.2001.280.3.f480.

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Endothelial dysfunction accompanies suboptimal glucose control in patients with diabetes mellitus. A hallmark of endothelial dysfunction is a deficiency in production or bioavailability of vascular nitric oxide (NO). Here we demonstrate that acute exposure of human endothelial cells to glucose, at levels found in plasma of diabetic patients, results in a significant blunting of NO responses to the endothelial nitric oxide synthase (eNOS) agonists bradykinin and A-23187. Monitoring of NO generation by purified recombinant bovine eNOS in vitro, using amperometric electrochemical detection and an NO-selective porphyrinic microelectrode, showed that glucose causes a progressive and concentration-dependent attenuation of detectable NO. Addition of glucose to pure NO solutions similarly elicited a sharp decrease in NO concentration, indicating that glucose promotes NO loss. Electrospray ionization-tandem mass spectrometry, using negative ion monitoring, directly demonstrated the occurrence of a covalent reaction involving unitary addition of NO (or a derived species) to glucose. Collectively, our findings reveal that hyperglycemia promotes the chemical inactivation of NO; this glucose-mediated NO loss may directly contribute to hypertension and endothelial dysfunction in diabetic patients.

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Lauer, Thomas, Petra Kleinbongard, and Malte Kelm. "Indexes of NO Bioavailability in Human Blood." Physiology 17, no. 6 (December 2002): 251–55. http://dx.doi.org/10.1152/nips.01405.2002.

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Disturbances of nitric oxide (NO) bioavailability may play a key role in vascular dysfunction and in the development of atherosclerotic lesions. Thus assessment of a reduced NO bioavailability in human circulation is of particular interest. Here we summarize potential biomarkers of NO availability in human blood and critically discuss their respective significance and application fields.

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Zhang, Yixuan, Stefan P. Janssens, Kirstin Wingler, Harald H. H. W. Schmidt, and An L. Moens. "Modulating endothelial nitric oxide synthase: a new cardiovascular therapeutic strategy." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 3 (September 2011): H634—H646. http://dx.doi.org/10.1152/ajpheart.01315.2010.

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The pathogenesis of many cardiovascular diseases is associated with reduced nitric oxide (NO) bioavailability and/or increased endothelial NO synthase (eNOS)-dependent superoxide formation. These findings support that restoring and conserving adequate NO signaling in the heart and blood vessels is a promising therapeutic intervention. In particular, modulating eNOS, e.g., through increasing the bioavailability of its substrate and cofactors, enhancing its transcription, and interfering with other modulators of eNOS pathway, such as netrin-1, has a high potential for effective treatments of cardiovascular diseases. This review provides an overview of the possibilities for modulating eNOS and how this may be translated to the clinic in addition to describing the genetic models used to study eNOS modulation.

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Neishi, Y., S. Mochizuki, T. Miyasaka, T. Kawamoto, T. Kume, R. Sukmawan, M. Tsukiji, et al. "Evaluation of bioavailability of nitric oxide in coronary circulation by direct measurement of plasma nitric oxide concentration." Proceedings of the National Academy of Sciences 102, no. 32 (July 28, 2005): 11456–61. http://dx.doi.org/10.1073/pnas.0501392102.

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Schmithorst, Vanessa J., Phillip S. Adams, Daryaneh Badaly, Vincent K. Lee, Julia Wallace, Nancy Beluk, Jodie K. Votava-Smith, et al. "Impaired Neurovascular Function Underlies Poor Neurocognitive Outcomes and Is Associated with Nitric Oxide Bioavailability in Congenital Heart Disease." Metabolites 12, no. 9 (September 19, 2022): 882. http://dx.doi.org/10.3390/metabo12090882.

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We use a non-invasive MRI proxy of neurovascular function (pnvf) to assess the ability of the vasculature to supply baseline metabolic demand, to compare pediatric and young adult congenital heart disease (CHD) patients to normal referents and relate the proxy to neurocognitive outcomes and nitric oxide bioavailability. In a prospective single-center study, resting-state blood-oxygen-level-dependent (BOLD) and arterial spin labeling (ASL) MRI scans were successfully obtained from 24 CHD patients (age = 15.4 ± 4.06 years) and 63 normal referents (age = 14.1 ± 3.49) years. Pnvf was computed on a voxelwise basis as the negative of the ratio of functional connectivity strength (FCS) estimated from the resting-state BOLD acquisition to regional cerebral blood flow (rCBF) as estimated from the ASL acquisition. Pnvf was used to predict end-tidal CO2 (PETCO2) levels and compared to those estimated from the BOLD data. Nitric oxide availability was obtained via nasal measurements (nNO). Pnvf was compared on a voxelwise basis between CHD patients and normal referents and correlated with nitric oxide availability and neurocognitive outcomes as assessed via the NIH Toolbox. Pnvf was shown as highly predictive of PETCO2 using theoretical modeling. Pnvf was found to be significantly reduced in CHD patients in default mode network (DMN, comprising the ventromedial prefrontal cortex and posterior cingulate/precuneus), salience network (SN, comprising the insula and dorsal anterior cingulate), and central executive network (CEN, comprising posterior parietal and dorsolateral prefrontal cortex) regions with similar findings noted in single cardiac ventricle patients. Positive correlations of Pnvf in these brain regions, as well as the hippocampus, were found with neurocognitive outcomes. Similarly, positive correlations between Pnvf and nitric oxide availability were found in frontal DMN and CEN regions, with particularly strong correlations in subcortical regions (putamen). Reduced Pnvf in CHD patients was found to be mediated by nNO. Mediation analyses further supported that reduced Pnvf in these regions underlies worse neurocognitive outcome in CHD patients and is associated with nitric oxide bioavailability. Impaired neuro-vascular function, which may be non-invasively estimated via combined arterial-spin label and BOLD MR imaging, is a nitric oxide bioavailability dependent factor implicated in adverse neurocognitive outcomes in pediatric and young adult CHD.

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Benson, Renée C., Karen A. Hardy, and Claudia R. Morris. "Arginase and Arginine Dysregulation in Asthma." Journal of Allergy 2011 (April 26, 2011): 1–12. http://dx.doi.org/10.1155/2011/736319.

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In recent years, evidence has accumulated indicating that the enzyme arginase, which converts L-arginine into L-ornithine and urea, plays a key role in the pathogenesis of pulmonary disorders such as asthma through dysregulation of L-arginine metabolism and modulation of nitric oxide (NO) homeostasis. Allergic asthma is characterized by airway hyperresponsiveness, inflammation, and remodeling. Through substrate competition, arginase decreases bioavailability of L-arginine for nitric oxide synthase (NOS), thereby limiting NO production with subsequent effects on airway tone and inflammation. By decreasing L-arginine bioavailability, arginase may also contribute to the uncoupling of NOS and the formation of the proinflammatory oxidant peroxynitrite in the airways. Finally, arginase may play a role in the development of chronic airway remodeling through formation of L-ornithine with downstream production of polyamines and L-proline, which are involved in processes of cellular proliferation and collagen deposition. Further research on modulation of arginase activity and L-arginine bioavailability may reveal promising novel therapeutic strategies for asthma.

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Balázs, N. "Transcutaneous carbon dioxide therapy improves the bioavailability of nitric oxide." Boletin Sociedad Española Hidrologia Medica 33, S1 (2018): 84. http://dx.doi.org/10.23853/bsehm.2018.0598.

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39

Gao, Ling, Yuh-Fen Pung, Jun Zhang, Peng Chen, Ting Wang, Min Li, Miguel Meza, Ligia Toro, and Hua Cai. "Sepiapterin reductase regulation of endothelial tetrahydrobiopterin and nitric oxide bioavailability." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 1 (July 2009): H331—H339. http://dx.doi.org/10.1152/ajpheart.00007.2009.

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Sepiapterin reductase (SPR) catalyzes the final step of tetrahydrobiopterin (H4B) biosynthesis and the first step of H4B regeneration from an exogenous precursor sepiapterin. Despite the potential significance of SPR in regulating H4B-dependent nitric oxide (NO•) production, the endothelium-specific sequence and functions of SPR remain elusive. We first cloned endothelial SPR cDNA from bovine aortic endothelial cells (Genebank: DQ978331). In cells transiently transfected with SPR gene, SPR activity (HPLC) was dramatically increased by 19-fold, corresponding to a significant increase in endothelial H4B content (HPLC) and NO• production (electron spin resonance). In vivo delivery of SPR gene significantly increased vascular SPR protein expression (mouse vs. bovine antibodies to differentiate endogenous vs. exogenous), activity, H4B content, and NO• production, as well as NO•-dependent vasorelaxation. In endothelial cells transfected with small interfering RNA specific for SPR, ∼87% of mRNA were attenuated (real-time quantitative RT-PCR), corresponding to a significant reduction in SPR protein expression and activity, which was associated with decreases in both intracellular H4B content and NO• level. Exogenous administration of sepiapterin to endothelial cells significantly upregulated H4B and NO• levels, which were attenuated by SPR RNA interference (RNAi). H4B-stimulated increase in NO• production, however, was SPR RNAi independent. GTP cyclohydrolase 1 expression and activity, as well as dihydrofolate reductase expression, were not affected by SPR RNAi, whereas dihydrofolate reductase activity was significantly downregulated. These data represent the first to study endothelial SPR functionally and clearly demonstrate an important role of endothelial SPR in modulating H4B and NO• bioavailability.

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Tsoukias, Nikolaos M. "Nitric Oxide Bioavailability in the Microcirculation: Insights from Mathematical Models." Microcirculation 15, no. 8 (January 2008): 813–34. http://dx.doi.org/10.1080/10739680802010070.

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La Favor, Justin D., Zongming Fu, Vidya Venkatraman, Trinity J. Bivalacqua, Jennifer E. Van Eyk, and Arthur L. Burnett. "Molecular Profile of Priapism Associated with Low Nitric Oxide Bioavailability." Journal of Proteome Research 17, no. 3 (February 12, 2018): 1031–40. http://dx.doi.org/10.1021/acs.jproteome.7b00657.

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Jain, Shilpa, and Mark T. Gladwin. "Arginine Metabolism and Nitric Oxide Bioavailability in Sickle Cell Disease." Journal of Pediatric Hematology/Oncology 32, no. 7 (October 2010): e247-e248. http://dx.doi.org/10.1097/mph.0b013e3181ec0b00.

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Shin, I. W., S. H. Ok, K. E. Park, J. T. Sohn, Y. K. Chung, and H. K. Lee. "Lipid emulsion increase blood pressure by decreasing nitric oxide bioavailability." European Journal of Anaesthesiology 30 (June 2013): 154–55. http://dx.doi.org/10.1097/00003643-201306001-00481.

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44

Davis, Joshua S., Christabelle J. Darcy, Tsin W. Yeo, Catherine Jones, Yvette R. McNeil, Dianne P. Stephens, David S. Celermajer, and Nicholas M. Anstey. "Asymmetric Dimethylarginine, Endothelial Nitric Oxide Bioavailability and Mortality in Sepsis." PLoS ONE 6, no. 2 (February 18, 2011): e17260. http://dx.doi.org/10.1371/journal.pone.0017260.

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Semenikhina, Marharyta, Mariia Stefanenko, Denisha R. Spires, Daria V. Ilatovskaya, and Oleg Palygin. "Nitric-Oxide-Mediated Signaling in Podocyte Pathophysiology." Biomolecules 12, no. 6 (May 25, 2022): 745. http://dx.doi.org/10.3390/biom12060745.

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Nitric oxide (NO) is a potent signaling molecule involved in many physiological and pathophysiological processes in the kidney. NO plays a complex role in glomerular ultrafiltration, vasodilation, and inflammation. Changes in NO bioavailability in pathophysiological conditions such as hypertension or diabetes may lead to podocyte damage, proteinuria, and rapid development of chronic kidney disease (CKD). Despite the extensive data highlighting essential functions of NO in health and pathology, related signaling in glomerular cells, particularly podocytes, is understudied. Several reports indicate that NO bioavailability in glomerular cells is decreased during the development of renal pathology, while restoring NO level can be beneficial for glomerular function. At the same time, the compromised activity of nitric oxide synthase (NOS) may provoke the formation of peroxynitrite and has been linked to autoimmune diseases such as systemic lupus erythematosus. It is known that the changes in the distribution of NO sources due to shifts in NOS subunits expression or modifications of NADPH oxidases activity may be linked to or promote the development of pathology. However, there is a lack of information about the detailed mechanisms describing the production and release of NO in the glomerular cells. The interaction of NO and other reactive oxygen species in podocytes and how NO-calcium crosstalk regulates glomerular cells’ function is still largely unknown. Here, we discuss recent reports describing signaling, synthesis, and known pathophysiological mechanisms mediated by the changes in NO homeostasis in the podocyte. The understanding and further investigation of these essential mechanisms in glomerular cells will facilitate the design of novel strategies to prevent or manage health conditions that cause glomerular and kidney damage.

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46

Govers, Roland, and Ton J. Rabelink. "Cellular regulation of endothelial nitric oxide synthase." American Journal of Physiology-Renal Physiology 280, no. 2 (February 1, 2001): F193—F206. http://dx.doi.org/10.1152/ajprenal.2001.280.2.f193.

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Renal function is highly dependent on endothelium-derived nitric oxide (NO). Several renal disorders have been linked to impaired NO bioavailability. The enzyme that is responsible for the synthesis of NO within the renal endothelium is endothelial NO synthase (eNOS). eNOS-mediated NO generation is a highly regulated cellular event, which is induced by calcium-mobilizing agonists and fluid shear stress. eNOS activity is regulated at the transcriptional level but also by a variety of modifications, such as acylation and phosphorylation, by its cellular localization, and by protein-protein interactions. The present review focuses on the complex regulation of eNOS within the endothelial cell.

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Gawrys, Jakub, Damian Gajecki, Ewa Szahidewicz-Krupska, and Adrian Doroszko. "Intraplatelet L-Arginine-Nitric Oxide Metabolic Pathway: From Discovery to Clinical Implications in Prevention and Treatment of Cardiovascular Disorders." Oxidative Medicine and Cellular Longevity 2020 (March 4, 2020): 1–11. http://dx.doi.org/10.1155/2020/1015908.

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Despite the development of new drugs and other therapeutic strategies, cardiovascular disease (CVD) remains still the major cause of morbidity and mortality in the world population. A lot of research, performed mostly in the last three decades, revealed an important correlation between “classical” demographic and biochemical risk factors for CVD, (i.e., hypercholesterolemia, hyperhomocysteinemia, smoking, renal failure, aging, diabetes, and hypertension) with endothelial dysfunction associated directly with the nitric oxide deficiency. The discovery of nitric oxide and its recognition as an endothelial-derived relaxing factor was a breakthrough in understanding the pathophysiology and development of cardiovascular system disorders. The nitric oxide synthesis pathway and its regulation and association with cardiovascular risk factors were a common subject for research during the last decades. As nitric oxide synthase, especially its endothelial isoform, which plays a crucial role in the regulation of NO bioavailability, inhibiting its function results in the increase in the cardiovascular risk pattern. Among agents altering the production of nitric oxide, asymmetric dimethylarginine—the competitive inhibitor of NOS—appears to be the most important. In this review paper, we summarize the role of L-arginine-nitric oxide pathway in cardiovascular disorders with the focus on intraplatelet metabolism.

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Hyduke, Daniel R., and James C. Liao. "Analysis of nitric oxide donor effectiveness in resistance vessels." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 5 (May 2005): H2390—H2399. http://dx.doi.org/10.1152/ajpheart.00990.2004.

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Decreased nitric oxide (NO) bioavailability is associated with a number of pathological conditions. Administration of a supplemental source of NO can counter the pathological effects arising from decreased NO bioavailability. A class of NO-nucleophile adducts that spontaneously release NO (NONOates) has been developed, and its members show promise as therapeutic sources of NO. Because the NONOates release NO spontaneously, a significant portion of the NO may be consumed by the myriad of NO reactive species present in the body. Here we develop a model to analyze the efficacy of NO delivery, by membrane-impermeable NONOates, in the resistance arterioles. Our model identifies three features of blood vessels that will enhance NONOate efficacy: 1) the amount of NO delivered to the abluminal region increases with lumen radius; 2) the presence of a flow-induced red blood cell-free zone will augment NO delivery; and 3) extravasation of the NONOate into the interstitial space will increase abluminal NO delivery. These results suggest that NONOates may be more effective in larger vessels and that NONOate efficacy can be altered by modifying permeability to the interstitial space.

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Mathru, Mali, Ruksana Huda, Daneshvari R. Solanki, Stephen Hays, and John D. Lang. "Inhaled Nitric Oxide Attenuates Reperfusion Inflammatory Responses in Humans." Anesthesiology 106, no. 2 (February 1, 2007): 275–82. http://dx.doi.org/10.1097/00000542-200702000-00015.

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Background Reduced bioavailability of endothelium-derived nitric oxide associated with reperfusion could potentially exacerbate the inflammatory response during reperfusion. Evidence suggests the pharmacologic effects of inhaled nitric oxide may extend beyond the pulmonary vasculature, and this is attributed to nitric oxide-derived complexes in blood that ultimately orchestrate antiinflammatory effects. In this study, the authors evaluated the potential for inhaled nitric oxide (80 ppm) to attenuate inflammation instigated by ischemia-reperfusion in a human model using patients undergoing knee surgery where a tourniquet was used to produce a bloodless surgical field. Methods Inhaled nitric oxide (80 ppm) was administered before tourniquet application and continued throughout reperfusion until the completion of surgery. Venous blood samples were collected before and after reperfusion, for the measurements of nitrate and nitrite, CD11b/CD18, soluble P-selectin, and lipid hydroperoxide. Muscle biopsies were obtained from the quadriceps muscle before skin closure and analyzed for myeloperoxide, conjugated dienes, and nuclear factor-kappaB translocation. Results Administration of inhaled nitric oxide (80 ppm) significantly attenuated the inflammatory response characterized by reduced expression of CD11b/CD18, P-selectin, and nuclear factor kappaB compared with the control group. This was accompanied by increased plasma levels of nitrate and nitrite and reduced oxidative stress. Conclusions Administration of inhaled nitric oxide at 80 ppm significantly reduces inflammation in lower extremity ischemia-reperfusion in humans. This observation supports the concept that during diseases characterized by dysfunction in nitric oxide metabolism, inhaled nitric oxide may be an effective therapy to replenish systemic nitric oxide, thus retarding inflammatory-mediated injury.

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Magenta, Alessandra, Simona Greco, Maurizio C. Capogrossi, Carlo Gaetano, and Fabio Martelli. "Nitric Oxide, Oxidative Stress, andp66ShcInterplay in Diabetic Endothelial Dysfunction." BioMed Research International 2014 (2014): 1–16. http://dx.doi.org/10.1155/2014/193095.

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Increased oxidative stress and reduced nitric oxide (NO) bioavailability play a causal role in endothelial cell dysfunction occurring in the vasculature of diabetic patients. In this review, we summarized the molecular mechanisms underpinning diabetic endothelial and vascular dysfunction. In particular, we focused our attention on the complex interplay existing among NO, reactive oxygen species (ROS), and one crucial regulator of intracellular ROS production,p66Shcprotein.

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