Journal articles: 'Nitric oxide resistance'

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Nathan, Carl. "Natural resistance and nitric oxide." Cell 82, no. 6 (September 1995): 873–76. http://dx.doi.org/10.1016/0092-8674(95)90019-5.

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Benzing, Albert, Torsten Loop, Georg Mols, and Klaus Geiger. "Unintended Inhalation of Nitric Oxide by Contamination of Compressed Air." Anesthesiology 91, no. 4 (October 1, 1999): 945. http://dx.doi.org/10.1097/00000542-199910000-00013.

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Background Compressed air from a hospital's central gas supply may contain nitric oxide as a result of air pollution. Inhaled nitric oxide may increase arterial oxygen tension and decrease pulmonary vascular resistance in patients with acute lung injury and acute respiratory distress syndrome. Therefore, the authors wanted to determine whether unintentional nitric oxide inhalation by contamination of compressed air influences arterial oxygen tension and pulmonary vascular resistance and interferes with the therapeutic use of nitric oxide. Methods Nitric oxide concentrations in the compressed air of a university hospital were measured continuously by chemiluminescence during two periods (4 and 2 weeks). The effects of unintended nitric oxide inhalation on arterial oxygen tension (n = 15) and on pulmonary vascular resistance (n = 9) were measured in patients with acute lung injury and acute respiratory distress syndrome by changing the source of compressed air of the ventilator from the hospital's central gas supply to a nitric oxide-free gas tank containing compressed air. In five of these patients, the effects of an additional inhalation of 5 ppm nitric oxide were evaluated. Results During working days, compressed air of the hospital's central gas supply contained clinically effective nitric oxide concentrations (> 80 parts per billion) during 40% of the time. Change to gas tank-supplied nitric oxide-free compressed air decreased the arterial oxygen tension by 10% and increased pulmonary vascular resistance by 13%. The addition of 5 ppm nitric oxide had a minimal effect on arterial oxygen tension and pulmonary vascular resistance when added to hospital-supplied compressed air but improved both when added to tank-supplied compressed air. Conclusions Unintended inhalation of nitric oxide increases arterial oxygen tension and decreases pulmonary vascular resistance in patients with acute lung injury and acute respiratory distress syndrome. The unintended nitric oxide inhalation interferes with the therapeutic use of nitric oxide.

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Lee, Alexandra, and Warwick Butt. "Nitric oxide: a new role in intensive care." Critical Care and Resuscitation 22, no. 1 (March 2, 2020): 72–79. http://dx.doi.org/10.51893/2020.1.sr1.

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Inhaled nitric oxide has been used for 30 years to improve oxygenation and decrease pulmonary vascular resistance. In the past 15 years, there has been increased understanding of the role of endogenous nitric oxide on cell surface receptors, mitochondria, and intracellular processes involving calcium and superoxide radicals. This has led to several animal and human experiments revealing a potential role for administered nitric oxide or nitric oxide donors in patients with systemic inflammatory response syndrome or ischaemia–reperfusion injury, and in patients for whom exposure of blood to artificial surfaces has occurred.

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Wu, Guoyao, and Cynthia J. Meininger. "Nitric oxide and vascular insulin resistance." BioFactors 35, no. 1 (January 2009): 21–27. http://dx.doi.org/10.1002/biof.3.

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Perez-Rojas, Jazmin M., Kamal M. Kassem, William H. Beierwaltes, Jeffrey L. Garvin, and Marcela Herrera. "Nitric oxide produced by endothelial nitric oxide synthase promotes diuresis." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 298, no. 4 (April 2010): R1050—R1055. http://dx.doi.org/10.1152/ajpregu.00181.2009.

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Extracellular fluid volume is highly regulated, at least in part, by peripheral resistance and renal function. Nitric oxide (NO) produced by NO synthase type 3 (NOS 3) in the nonrenal vasculature may promote fluid retention by reducing systemic vascular resistance and arterial pressure. In contrast, NO produced by renal NOS 3 promotes water excretion by reducing renal vascular resistance, increasing glomerular filtration, and inhibiting reabsorption along the nephron. Thus, the net effect of NO from NOS 3 on urinary volume (UV) is unclear. We hypothesized that NO produced by NOS 3 promotes water excretion primarily due to renal tubular effects. We gave conscious wild-type and NOS 3 −/− mice an acute volume load and measured UV, blood pressure, plasma renin concentration (PRC), Na+, vasopressin, and urinary Na+ and creatinine concentrations. To give the acute volume load, we trained mice to drink a large volume of water while in metabolic cages. On the day of the experiment, water was replaced with 1% sucrose, and mice had access to it for 1 h. Volume intake was similar in both groups. Over 3 h, wild-type mice excreted 62 ± 10% of the volume load, but NOS 3 −/− excreted only 42 ± 5% ( P < 0.05). Blood pressure in NOS 3 −/− was 118 ± 3 compared with 110 ± 2 mmHg in wild-type mice ( P < 0.05), but it did not change following volume load in either strain. PRC, vasopressin, and glomerular filtration rate were similar between groups. Urinary Na+ excretion was 49.3 ± 7.0 in wild-type vs. 37.8 ± 6.4 μmol/3 h in NOS 3 −/− mice ( P < 0.05). Bumetanide administration eliminated the difference in volume excretion between wild-type and NOS 3 −/− mice. We conclude that 1) NO produced by NOS 3 promotes water and Na+ excretion and 2) the renal epithelial actions of NO produced by NOS 3 supersede the systemic and renal vascular actions.

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Ramya K, Gowri Sethu, and Dhanasekar T. "Is Nitric oxide the missing link in glucose homeostasis? A study on correlation of Nitric oxide and Insulin Resistance in Obstructive Sleep Apnoea." International Journal of Research in Pharmaceutical Sciences 10, no. 2 (April 15, 2019): 820–25. http://dx.doi.org/10.26452/ijrps.v10i2.258.

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Nitric oxide is associated with glucose homeostasis. An independent relationship between Nitric oxide and insulin resistance in Prediabetic and Obstructive sleep apnea patients without pre-existing diabetes mellitus are equivocally linked to increased risk of type II diabetes. A reciprocal relationship seems to exist between nitric oxide and insulin resistance. Aim of this present study is to determine relationship between nitric oxide and glucose parameters in control, prediabetic and Obstructive sleep apnea. A cross sectional study was performed in 150. They were divided into, group I (control), group II (prediabetics) and group III (OSA). Fasting blood sugar (FBS), fasting insulin, HbA1c and nitric oxide were measured in these subjects and insulin resistance calculated by HOMA-IR. Data was analyzed statistically using Pearson’s correlation coefficient analysis, the significant value being P<0.05. Negative correlation was observed between the NO and insulin resistance in prediabetic (r=-0.627, P =<0.001) and OSA (r= -0.416, P=0.003) respectively. Nitric oxide is significantly inversely associated with insulin resistance in Prediabetic and Obstructive sleep apnea.

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Green, Shawn J., Libia F. Scheller, Michael A. Marletta, Matthew C. Seguin, Francis W. Klotz, Mike Slayter, Barbara J. Nelson, and Carol A. Nacy. "Nitric oxide: Cytokine-regulation of nitric oxide in host resistance to intracellular pathogens." Immunology Letters 43, no. 1-2 (December 1994): 87–94. http://dx.doi.org/10.1016/0165-2478(94)00158-8.

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Kuzhebaeva, U., Irina Donnik, Maksim Petropavlovskiy, S. Kanatbaev, and Birzhan Nurgaliev. "Nitric oxide as an indicator for assessing the resistance and susceptibility of cattle to leukemia." Agrarian Bulletin of the 213, no. 10 (November 26, 2021): 48–54. http://dx.doi.org/10.32417/1997-4868-2021-213-10-48-54.

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Abstract. The role of allelic variability of inducible nitric oxide synthase (iNOS) is significant in the study of the resistance and susceptibility of animals to leukemia infection. After analyzing the literature data, it can be stated that in the iNOS gene, allele A (with genotype AA) is responsible for resistance to the leukemia virus, and allele B (with genotype BB) is responsible for susceptibility. This is due to the frequency of occurrence of alleles and their genotypes of the polymorphic marker AN13-1 of the inducibeal nitric oxide synthase gene. The iNOS gene is capable of producing a large amount of nitric oxide, compared to other isoforms. In turn, nitric oxide causes death or can stop the growth of pathogenic microorganisms, including viruses. The purpose of this work is to further study nitric oxide as an indicator for determining the resistance and susceptibility of animals to leukemia, as well as the selection of specific primers for PCR-PDRF used in genotyping. Methods. The iNOS gene sequence was analyzed and a pair of specific primers were selected and synthesized using the Vector NTI program. Scientific novelty of this work lies in the fact that we have selected specific primers that are important for the analysis of cattle genotyping by allelic variants of the polymorphic marker AH13-1 of the iNOS gene. Results. Based on this work, a pair of primers iNOSF_new and iNOSR_new, with a calculated annealing temperature of 52 °C, were selected and synthesized, giving an amplicon with a length of 186 bp. The amplicon contains a polymorphic site that distinguishes the A and B alleles. During PCR-RFLP, the following genotype-specific fragments are formed: AA-47/139 bp; AB -186/139/47 bp; BB-186 bp.

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Bigatello, Luca M., and William E. Hurford. "Inhaled nitric oxide and pulmonary vascular resistance." Critical Care Medicine 27, no. 9 (September 1999): 2060–61. http://dx.doi.org/10.1097/00003246-199909000-00075.

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Mohteshamzadeh, Mobin, and T. H. Tomas. "HYPERTENSION, INSULIN RESISTANCE AND NITRIC OXIDE SYNTHASE." Journal of Hypertension 22, Suppl. 1 (February 2004): S49. http://dx.doi.org/10.1097/00004872-200402001-00199.

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Spiro, Stephen. "An alternative route to nitric oxide resistance." Molecular Microbiology 77, no. 1 (May 4, 2010): 6–10. http://dx.doi.org/10.1111/j.1365-2958.2010.07195.x.

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Elahi, Shokrollah, Gerald Pang, Robert B. Ashman, and Robert Clancy. "Nitric oxide-enhanced resistance to oral candidiasis." Immunology 104, no. 4 (December 2001): 447–54. http://dx.doi.org/10.1046/j.1365-2567.2001.01331.x.

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Angiolillo, Dominick J., and Davide Capodanno. "Targeting Platelet Nitric Oxide Resistance With Ramipril." Journal of the American College of Cardiology 60, no. 10 (September 2012): 895–97. http://dx.doi.org/10.1016/j.jacc.2012.02.046.

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Uese, Kei-ichiro, Fukiko Ichida, Shin-ichi Tsubata, Ikuo Hashimoto, Yuji Hamamichi, Kazuaki Fukahara, Arata Murakami, and Toshio Miyawaki. "Oral prostacyclin enhances the pulmonary vasodilatory effect of nitric oxide in children with pulmonary hypertension." Cardiology in the Young 7, no. 4 (October 1997): 362–69. http://dx.doi.org/10.1017/s1047951100004340.

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AbstractTo evaluate the potential efficacy of the combined administration of inhaled nitric oxide and oral beraprost sodium in producing pulmonary vasodilation, we studied 20 patients with pulmonary hypertension during cardiac catheterization. We also evaluated some of the mechanisms of vasodilation under these circumstances by investigating the levels of cyclic GMP and AMP in the pulmonary venous blood. A significant decrease in pulmonary vascular resistance was observed after the administration of nitric oxide (−37 ± 6%, p<0.01), and more intense decrease was observed after the combined administration of nitric oxide and beraprost sodium (−46 ± 6%, p<0.05). In addition, the ratio of pulmonary-to-systemic resistance also decreased to a greater extent with combined administration than with nitric oxide alone (−34 ± 6% vs −42 ± 7%, p<0.05). Conversely, systemic vascular resistance showed no change, neither after loading with nitric oxide nor after combined administration. Although equivalent increases in levels of cyclic GMP were observed after inhalation of nitric and the combined administration (mean 78% vs 65%), greater increases in levels of cyclic AMP were observed with the combined use (mean 15% vs 69%). Combined treatment with nitric oxide and beraprost sodium may prove markedly beneficial in patients with primary and postoperative pulmonary hypertension who do not respond adequately to inhalation of nitric oxide alone or conventional modes of treatment.

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Lautt, W. Wayne. "The HISS story overview: a novel hepatic neurohumoral regulation of peripheral insulin sensitivity in health and diabetes." Canadian Journal of Physiology and Pharmacology 77, no. 8 (September 1, 1999): 553–62. http://dx.doi.org/10.1139/y99-067.

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Data are reviewed that are consistent with the following working hypothesis that proposes a novel mechanism regulating insulin sensitivity, which when nonfunctional, leads to severe insulin resistance. Postprandial elevation in insulin levels activates a hepatic parasympathetic reflex release of a putative hepatic insulin-sensitizing substance (HISS), which activates glucose uptake at skeletal muscle. Insulin causes HISS release in fed but not fasted animals. The reflex is mediated by acetylcholine and involves release of nitric oxide in the liver. Interruption of the release of HISS is achieved by surgical denervation of the anterior hepatic nerve plexus, muscarinic receptor blockade, or nitric oxide synthase antagonism and leads to immediate severe insulin resistance. The nitric oxide donor, SIN-1, reverses L-NAME-induced insulin resistance. Denervation-induced insulin resistance is reversed by intraportal but not intravenous administration of acetylcholine or SIN-1. Liver disease is often associated with insulin resistance; the bile duct ligation model of liver disease results in parasympathetic neuropathy and insulin resistance that is reversed by intraportal acetylcholine. Possible relevance of this HISS-dependent control of insulin action to insulin resistance in diabetes, liver disease, and obesity is discussed.Key words: insulin resistance, parasympathetic nerves, liver, obesity, nitric oxide.

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Russell, Tiffany M., Mahan Gholam Azad, and Des R. Richardson. "The Relationship of Glutathione-S-Transferase and Multi-Drug Resistance-Related Protein 1 in Nitric Oxide (NO) Transport and Storage." Molecules 26, no. 19 (September 24, 2021): 5784. http://dx.doi.org/10.3390/molecules26195784.

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Nitric oxide is a diatomic gas that has traditionally been viewed, particularly in the context of chemical fields, as a toxic, pungent gas that is the product of ammonia oxidation. However, nitric oxide has been associated with many biological roles including cell signaling, macrophage cytotoxicity, and vasodilation. More recently, a model for nitric oxide trafficking has been proposed where nitric oxide is regulated in the form of dinitrosyl-dithiol-iron-complexes, which are much less toxic and have a significantly greater half-life than free nitric oxide. Our laboratory has previously examined this hypothesis in tumor cells and has demonstrated that dinitrosyl-dithiol-iron-complexes are transported and stored by multi-drug resistance-related protein 1 and glutathione-S-transferase P1. A crystal structure of a dinitrosyl-dithiol-iron complex with glutathione-S-transferase P1 has been solved that demonstrates that a tyrosine residue in glutathione-S-transferase P1 is responsible for binding dinitrosyl-dithiol-iron-complexes. Considering the roles of nitric oxide in vasodilation and many other processes, a physiological model of nitric oxide transport and storage would be valuable in understanding nitric oxide physiology and pathophysiology.

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Bouwmeester, J. Christopher, Israel Belenkie, Nigel G. Shrive, and John V. Tyberg. "Partitioning pulmonary vascular resistance using the reservoir-wave model." Journal of Applied Physiology 115, no. 12 (December 15, 2013): 1838–45. http://dx.doi.org/10.1152/japplphysiol.00750.2013.

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The conventional determination of pulmonary vascular resistance does not indicate which vascular segments contribute to the total resistance of the pulmonary circulation. Using measurements of pressure and flow, the reservoir-wave model can be used to partition total pulmonary vascular resistance into arterial, microcirculation, and venous components. Changes to these resistance components are investigated during hypoxia and inhaled nitric oxide, volume loading, and positive end-expiratory pressure. The reservoir-wave model defines the pressure of a volume-related reservoir and the asymptotic pressure. The mean values of arterial and venous reservoir pressures and arterial and venous asymptotic pressures define a series of resistances between the main pulmonary artery and the pulmonary veins: the resistance of large and small arteries, the microcirculation, and veins. In 11 anaesthetized, open-chest dogs, pressure and flow were measured in the main pulmonary artery and a single pulmonary vein. Volume loading reduced each vascular resistance component, whereas positive end-expiratory pressure only increased microcirculation resistance. Hypoxia increased the resistance of small arteries and veins, whereas nitric oxide only decreased small-artery resistance significantly. The reservoir-wave model provides a novel method to deconstruct total pulmonary vascular resistance. The results are consistent with the expected physiological responses of the pulmonary circulation and provide additional information regarding which segments of the pulmonary circulation react to hypoxia and nitric oxide.

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Baylis, C., J. Harvey, and K. Engels. "Acute nitric oxide blockade amplifies the renal vasoconstrictor actions of angiotension II." Journal of the American Society of Nephrology 5, no. 2 (August 1994): 211–14. http://dx.doi.org/10.1681/asn.v52211.

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The tone in the renal vasculature is determined by the balance between vasoconstrictor and vasodilator agents. In this study, the effect on renal function was investigated when the acute blockade of the endogenous nitric oxide system was superimposed on a state of high circulating angiotensin II. Studies were conducted in the conscious, unstressed rat measuring renal function before and during acute systemic nitric oxide blockade with nitro-L-arginine methyl ester and with or without concomitant angiotensin II infusion. Nitric oxide blockade alone, in the presence of normal, unstimulated levels of endogenous angiotensin II, caused a large rise in blood pressure and a doubling of renal vascular resistance. The infusion of angiotensin II alone produced a mild rise in systemic blood pressure and a small (30%) rise in renal vascular resistance. When nitric oxide blockade was combined with angiotensin II infusion, the rise in blood pressure was similar to that produced by nitric oxide blockade alone but the increase in renal vascular resistance was much greater (350%), leading to marked declines in renal function. These studies demonstrate that when angiotensin II levels are acutely elevated and are controlling renal vascular tone, nitric oxide is essential for the maintenance of adequate renal perfusion and function.

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Duke, Trevor, Mike South, and Alastair Stewart. "Altered activation of the L-arginine nitric oxide pathway during and after cardiopulmonary bypass." Perfusion 12, no. 6 (December 1997): 405–10. http://dx.doi.org/10.1177/026765919701200609.

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The serum concentrations of nitrogen oxides, the stable metabolites of nitric oxide, were measured in 61 children during and after cardiopulmonary bypass (CPB) for surgery of congenital heart disease. Overall, there was a small reduction in serum nitrogen oxide concentrations during CPB, from a median of 27.5 (interquartile range 16.6-55.7) to 26.4 (15.3-40.6) μmol/l, followed by an increase in the following 24 h to 33.1 (21.3-46.7) μmol/l. The largest postoperative increases in nitrogen oxides occurred in children who developed renal impairment, or were treated with nitrovasodilators. There was no relationship between changes in serum nitrogen oxides intraoperatively and early changes in pulmonary vascular resistance, and a weak positive relationship between changes in serum nitrogen oxides and early postoperative changes in cardiac index ( r2 = 0.09, p = 0.04). We found no evidence for increased activation of the L-arginine nitric oxide pathway during CPB; and the reduction in nitric oxide metabolites that occurred during CPB were of doubtful significance to pulmonary or systemic haemodynamic changes in the postoperative period.

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Tschudi, M., V. Richard, F. R. Buhler, and T. F. Luscher. "Importance of endothelium-derived nitric oxide in porcine coronary resistance arteries." American Journal of Physiology-Heart and Circulatory Physiology 260, no. 1 (January 1, 1991): H13—H20. http://dx.doi.org/10.1152/ajpheart.1991.260.1.h13.

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Endothelial cells regulate vascular tone through the release of nitric oxide and other relaxing factors. The role of these substances was studied in isolated intramyocardial porcine coronary resistance arteries suspended in myographs for isometric tension recording. The inhibitor of nitric oxide formation NG-monomethyl-L-arginine (L-NMMA; 10(-7)-10(-4)M), but not D-NMMA, caused endothelium-dependent contractions that could be reversed by L-arginine but not by D-arginine. In preparations with endothelium, L-NMMA potentiated the contractions induced by acetylcholine and the relaxations to 3-morpholino-sydnonimine. Under both conditions, the effect of endothelial removal was slightly more pronounced than that of L-NMMA. Bradykinin, serotonin, and the alpha 2-adrenergic agonist clonidine evoked endothelium-dependent relaxations. L-NMMA as well as the inhibitor of guanylate cyclase methylene blue (10(-5) M) prevented the relaxations induced by clonidine, reduced those to serotonin, but hardly affected those to bradykinin. Thus, in porcine coronary resistance arteries, endothelium-derived nitric oxide is continuously produced from L-arginine. Endothelium-dependent relaxations to clonidine are fully mediated and those to serotonin partially mediated by nitric oxide; its release does not involve a Gi protein. An endothelium-derived relaxing factor different from nitric oxide must mediate the relaxations to bradykinin and contribute to those evoked by serotonin.

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Nesic, V. S., V. Z. Djordjevic, V. Tomic-Spiric, Z. R. Dudvarski, I. A. Soldatovic, and N. A. Arsovic. "Measuring nasal nitric oxide in allergic rhinitis patients." Journal of Laryngology & Otology 130, no. 11 (November 2016): 1064–71. http://dx.doi.org/10.1017/s0022215116009087.

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AbstractObjective:This study aimed to compare two sampling methods for nasal nitric oxide in healthy individuals and allergic rhinitis patients, and to examine the within-subject reliability of nasal nitric oxide measurement.Methods:The study included 23 allergic rhinitis patients without concomitant asthma and 10 healthy individuals. For all participants, nitric oxide levels were measured non-invasively from the lungs through the mouth (i.e. the oral fractional exhaled nitric oxide) and the nose. Nasal nitric oxide was measured by two different methods: (1) nasal aspiration via one nostril during breath holding and (2) single-breath quiet exhalation against resistance through a tight facemask (i.e. the nasal fractional exhaled nitric oxide).Results:Compared with healthy participants, allergic rhinitis patients had significantly higher average oral and nasal nitric oxide levels. All methods of nitric oxide measurement had excellent reliability.Conclusion:Nasal nitric oxide measurement is a useful and reliable clinical tool for diagnosing allergic rhinitis in patients without asthma in an out-patient setting.

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Hjoberg, Josephine, Stephanie Shore, Lester Kobzik, Shoji Okinaga, Arlene Hallock, Joseph Vallone, Venkat Subramaniam, et al. "Expression of nitric oxide synthase-2 in the lungs decreases airway resistance and responsiveness." Journal of Applied Physiology 97, no. 1 (July 2004): 249–59. http://dx.doi.org/10.1152/japplphysiol.01389.2003.

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Individuals with asthma have increased levels of nitric oxide in their exhaled air. To explore its role, we have developed a regulatable transgenic mouse capable of overexpressing inducible nitric oxide synthase in a lung-specific fashion. The CC10-rtTA-NOS-2 mouse contains two transgenes, a reverse tetracycline transactivator under the control of the Clara cell protein promoter and the mouse nitric oxide synthase-2 (NOS-2) coding region under control of a tetracycline operator. Addition of doxycycline to the drinking water of CC10-rtTA-NOS-2 mice causes an increase in nitric oxide synthase-2 that is largely confined to the airway epithelium. The fraction of expired nitric oxide increases over the first 24 h from ∼10 parts per billion to a plateau of ∼20 parts per billion. There were no obvious differences between CC10-rtTA-NOS-2 mice, with or without doxycycline, and wild-type mice in lung histology, bronchoalveolar protein, total cell count, or count differentials. However, airway resistance was lower in CC10-rtTA-NOS-2 mice with doxycycline than in CC10-rtTA-NOS-2 mice without doxycycline or wild-type mice with doxycycline. Moreover, doxycycline-treated CC10-rtTA-NOS-2 mice were hyporesponsive to methacholine compared with other groups. These data suggest that increased nitric oxide in the airways has no proinflammatory effects per se and may have beneficial effects on pulmonary function.

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Acharya, R., P. Patra, N. Chakraborty, N. S. Gupta, and K. Acharya. "Footprint of Nitric oxide in induced systemic resistance." NBU Journal of Plant Sciences 7, no. 1 (2013): 55–61. http://dx.doi.org/10.55734/nbujps.2013.v07i01.008.

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Nitric oxide (NO) is a potent signaling molecule with diverse physiological functions in plants. Several rhizobacterial strains may have capacity to induce systemic resistance in (ISR) plants but how far the biochemical mechanisms in which No participates in this signaling pathway is still an open question. The present study have shown in Pseudomonas aeruginosa WS-1 mediated ISR inducing system in Catharanthus roseus induces defense enzyme and phenolics and also showed a two fold increase in NO production when challenge with Alternaria alternata. Furthermore, NO donor treatment in the host produced same defense molecules in a comparable manner. From those observations it is suggested that NO might have possible signaling role in ISR during crosstalk between the ISR inducing agent and pathogen within the host system.

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Girotti, Albert W. "Nitric Oxide‐Mediated Resistance to Antitumor Photodynamic Therapy." Photochemistry and Photobiology 96, no. 3 (November 7, 2019): 500–505. http://dx.doi.org/10.1111/php.13163.

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Turchi, J. J. "Nitric oxide and cisplatin resistance: NO easy answers." Proceedings of the National Academy of Sciences 103, no. 12 (March 13, 2006): 4337–38. http://dx.doi.org/10.1073/pnas.0601001103.

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Grosser, Melinda R., Andy Weiss, Lindsey N. Shaw, and Anthony R. Richardson. "Regulatory Requirements for Staphylococcus aureus Nitric Oxide Resistance." Journal of Bacteriology 198, no. 15 (May 16, 2016): 2043–55. http://dx.doi.org/10.1128/jb.00229-16.

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ABSTRACTThe ability ofStaphylococcus aureusto resist host innate immunity augments the severity and pervasiveness of its pathogenesis. Nitric oxide (NO˙) is an innate immune radical that is critical for the efficient clearance of a wide range of microbial pathogens. Exposure of microbes to NO˙ typically results in growth inhibition and induction of stress regulons.S. aureus, however, induces a metabolic state in response to NO˙ that allows for continued replication and precludes stress regulon induction. The regulatory factors mediating this distinctive response remain largely undefined. Here, we employ a targeted transposon screen and transcriptomics to identify and characterize five regulons essential for NO˙ resistance inS. aureus: three virulence regulons not formerly associated with NO˙ resistance, SarA, CodY, and Rot, as well as two regulons with established roles, Fur and SrrAB. We provide new insights into the contributions of Fur and SrrAB during NO˙ stress and show that theS. aureusΔsarAmutant, the most sensitive of the newly identified mutants, exhibits metabolic dysfunction and widespread transcriptional dysregulation following NO˙ exposure. Altogether, our results broadly characterize the regulatory requirements for NO˙ resistance inS. aureusand suggest an intriguing overlap between the regulation of NO˙ resistance and virulence in this well-adapted human pathogen.IMPORTANCEThe prolific human pathogenStaphylococcus aureusis uniquely capable of resisting the antimicrobial radical nitric oxide (NO˙), a crucial component of the innate immune response. However, a complete understanding of howS. aureusregulates an effective response to NO˙ is lacking. Here, we implicate three central virulence regulators, SarA, CodY, and Rot, as major players in theS. aureusNO˙ response. Additionally, we elaborate on the contribution of two regulators, SrrAB and Fur, already known to play a crucial role inS. aureusNO˙ resistance. Our study sheds light on a unique facet ofS. aureuspathogenicity and demonstrates that the transcriptional response ofS. aureusto NO˙ is highly pleiotropic and intrinsically tied to metabolism and virulence regulation.

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Bishop, Amy, John C. Marquis, Neil R. Cashman, and Bruce Demple. "Adaptive resistance to nitric oxide in motor neurons." Free Radical Biology and Medicine 26, no. 7-8 (April 1999): 978–86. http://dx.doi.org/10.1016/s0891-5849(98)00284-6.

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Małolepsza, Urszula, and Sylwia Różalska. "Nitric oxide and hydrogen peroxide in tomato resistance." Plant Physiology and Biochemistry 43, no. 6 (June 2005): 623–35. http://dx.doi.org/10.1016/j.plaphy.2005.04.002.

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Privett, Benjamin J., Angela D. Broadnax, Susanne J. Bauman, Daniel A. Riccio, and Mark H. Schoenfisch. "Examination of bacterial resistance to exogenous nitric oxide." Nitric Oxide 26, no. 3 (March 2012): 169–73. http://dx.doi.org/10.1016/j.niox.2012.02.002.

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Mutchler, Stephanie M., and Adam C. Straub. "Compartmentalized nitric oxide signaling in the resistance vasculature." Nitric Oxide 49 (September 2015): 8–15. http://dx.doi.org/10.1016/j.niox.2015.05.003.

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Hinder, Frank, Michael Booke, Lillian D. Traber, and Daniel L. Traber. "Nitric oxide and endothelial permeability." Journal of Applied Physiology 83, no. 6 (December 1, 1997): 1941–46. http://dx.doi.org/10.1152/jappl.1997.83.6.1941.

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Hinder, Frank, Michael Booke, Lillian D. Traber, and Daniel L. Traber. Nitric oxide and endothelial permeability. J. Appl. Physiol. 83(6): 1941–1946, 1997.—Nitric oxide synthase inhibition reverses systemic vasodilation during sepsis but may increase endothelial permeability. To assess adverse effects on the pulmonary vasculature, 12 sheep were chronically instrumented with lung lymph fistulas and hydraulic pulmonary venous occluders. Escherichia coli endotoxin (lipopolysaccharide; 10 ng ⋅ kg−1 ⋅ min−1) was continuously infused for 32 h. After 24 h, six animals received 25 mg/kg of N ω-nitro-l-arginine methyl ester (l-NAME), and six received saline. All sheep developed a hyperdynamic circulatory response and elevated lymph flows by 24 h of lipopolysaccharide infusion. l-NAME reversed systemic vasodilation, increased pre- and postcapillary pulmonary vascular resistance index, pulmonary arterial pressure, and, transiently, effective pulmonary capillary pressure. Lung lymph flows were not different between groups at 24 h or thereafter. Calculated as changes from baseline, however, lung lymph flow was higher in thel-NAME group than in the control animals, with a trend toward lower lymph-to-plasma protein concentration ratio at 25 h. Permeability analysis at 32 h by the venous occlusion technique showed normal reflection coefficients and elevated filtration coefficients without differences between groups. Reversal by l-NAME of the systemic vasodilation during endotoxemia was associated with high pulmonary vascular resistance without evidence of impaired pulmonary endothelial barrier function.

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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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Rocco, Nicole M., John C. Carmen, and Bruce S. Klein. "Blastomyces dermatitidis Yeast Cells Inhibit Nitric Oxide Production by Alveolar Macrophage Inducible Nitric Oxide Synthase." Infection and Immunity 79, no. 6 (March 28, 2011): 2385–95. http://dx.doi.org/10.1128/iai.01249-10.

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ABSTRACTThe ability of pathogens to evade host antimicrobial mechanisms is crucial to their virulence. The dimorphic fungal pathogenBlastomyces dermatitidiscan infect immunocompetent patients, producing a primary pulmonary infection that can later disseminate to other organs.B. dermatitidispossesses a remarkable ability to resist killing by alveolar macrophages. To date, no mechanism to explain this resistance has been described. Here, we focus on macrophage production of the toxic molecule nitric oxide as a potential target of subversion byB. dermatitidisyeast cells. We report thatB. dermatitidisyeast cells reduce nitric oxide levels in the supernatants of activated alveolar macrophages. This reduction is not due to detoxification of nitric oxide, but rather to suppression of macrophage nitric oxide production. We show thatB. dermatitidisyeast cells do not block upregulation of macrophage inducible nitric oxide synthase (iNOS) expression or limit iNOS access to its arginine substrate. Instead,B. dermatitidisyeast cells appear to inhibit iNOS enzymatic activity. Further investigation into the genetic basis of this potential virulence mechanism could lead to the identification of novel antifungal drug targets.

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Aramide Modupe Dosunmu-Ogunbi, Atinuke, Joseph C. Galley, Shuai Yuan, Heidi M. Schmidt, Katherine C. Wood, and Adam C. Straub. "Redox Switches Controlling Nitric Oxide Signaling in the Resistance Vasculature and Implications for Blood Pressure Regulation: Mid-Career Award for Research Excellence 2020." Hypertension 78, no. 4 (October 2021): 912–26. http://dx.doi.org/10.1161/hypertensionaha.121.16493.

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The arterial resistance vasculature modulates blood pressure and flow to match oxygen delivery to tissue metabolic demand. As such, resistance arteries and arterioles have evolved a series of highly orchestrated cell-cell communication mechanisms between endothelial cells and vascular smooth muscle cells to regulate vascular tone. In response to neurohormonal agonists, release of several intracellular molecules, including nitric oxide, evokes changes in vascular tone. We and others have uncovered novel redox switches in the walls of resistance arteries that govern nitric oxide compartmentalization and diffusion. In this review, we discuss our current understanding of redox switches controlling nitric oxide signaling in endothelial and vascular smooth muscle cells, focusing on new mechanistic insights, physiological and pathophysiological implications, and advances in therapeutic strategies for hypertension and other diseases.

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Cremona, George, Tim Higenbottam, Motoshi Takao, Edward A. Bower, and Leslie W. Hall. "Nature and site of action of endogenous nitric oxide in vasculature of isolated pig lungs." Journal of Applied Physiology 82, no. 1 (January 1, 1997): 23–31. http://dx.doi.org/10.1152/jappl.1997.82.1.23.

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Cremona, George, Tim Higenbottam, Motoshi Takao, Edward A. Bower, and Leslie W. Hall. Nature and site of action of endogenous nitric oxide in vasculature of isolated pig lungs. J. Appl. Physiol. 82(1): 23–31, 1997.—The site of action of endogenous and exogenous nitric oxide (NO) in isolated pig lungs was investigated by using arterial, double, and venous occlusion, which allowed precapillary, postcapillary, and venous segments to be partitioned into arterial, precapillary, postcapillary, and venous segments. N G-nitro-l-arginine (l-NNA; 10−5 M) increased resistance in the arterial (35 ± 6.6%, P = 0.003), precapillary (39.3 ± 5.1%, P = 0.001), and venous (18.3 ± 4.8%, P = 0.01) segments, respectively. Sodium nitroprusside (10−5 M) and NO (80 parts/million) reversed the effects ofl-NNA. Total pulmonary vascular resistance fell with increasing flow, due to a fall in precapillary resistance and dynamic resistance, and was significantly lower than mean total resistance.l-NNA increased the resistances but did not alter the pattern of the pressure-flow relationships. It is concluded that, in isolated pig lungs, the effect of endogenous NO seems to be dependent on flow in the arterial segment and independent of flow in the precapillary segment, but variation of its release does not appear to be fundamental to accommodation to changes in steady flow.

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Kraus, Raymond M., Joseph A. Houmard, William E. Kraus, Charles J. Tanner, Joseph R. Pierce, Myung Dong Choi, and Robert C. Hickner. "Obesity, insulin resistance, and skeletal muscle nitric oxide synthase." Journal of Applied Physiology 113, no. 5 (September 1, 2012): 758–65. http://dx.doi.org/10.1152/japplphysiol.01018.2011.

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The molecular mechanisms responsible for impaired insulin action have yet to be fully identified. Rodent models demonstrate a strong relationship between insulin resistance and an elevation in skeletal muscle inducible nitric oxide synthase (iNOS) expression; the purpose of this investigation was to explore this potential relationship in humans. Sedentary men and women were recruited to participate (means ± SE: nonobese, body mass index = 25.5 ± 0.3 kg/m2, n = 13; obese, body mass index = 36.6 ± 0.4 kg/m2, n = 14). Insulin sensitivity was measured using an intravenous glucose tolerance test with the subsequent modeling of an insulin sensitivity index (SI). Skeletal muscle was obtained from the vastus lateralis, and iNOS, endothelial nitric oxide synthase (eNOS), and neuronal nitric oxide synthase (nNOS) content were determined by Western blot. SI was significantly lower in the obese compared with the nonobese group (∼43%; P < 0.05), yet skeletal muscle iNOS protein expression was not different between nonobese and obese groups. Skeletal muscle eNOS protein was significantly higher in the nonobese than the obese group, and skeletal muscle nNOS protein tended to be higher ( P = 0.054) in the obese compared with the nonobese group. Alternative analysis based on SI (high and low tertile) indicated that the most insulin-resistant group did not have significantly more skeletal muscle iNOS protein than the most insulin-sensitive group. In conclusion, human insulin resistance does not appear to be associated with an elevation in skeletal muscle iNOS protein in middle-aged individuals under fasting conditions.

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Mengxi, Wang, Xu Na, Zhou Renjie, Wu Jing, and Lei Hong. "Sesamin Ameliorates Insulin Resistance Induced by High Glucose/High Insulin in Hepatic L02 Cells." Current Topics in Nutraceutical Research 18, no. 1 (July 16, 2018): 70–74. http://dx.doi.org/10.37290/ctnr2641-452x.18:70-74.

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In this study, the antioxidant effect of sesamin on insulin resistance in hepatic L02 cells induced by high glucose/high insulin was investigated. Results showed that treatment with sesamin (200, 100 μg/ml) increased the cell viability, activity of superoxide dismutase and glutathione peroxidase, and the content of reduced glutathione of L02 hepatocyte model of insulin-resistance. Moreover, treatment with sesamin decreased the content of malondialdehyde, production of nitric oxide, and the activity of nitric oxide synthase, inducible nitric oxide synthase, and gene expression levels of c-Jun NH2-terminal kinase significantly. The destructive change of hepatic L02 cells was ameliorated when treated with sesamin under microscopic observation. In conclusion, sesamin has anti-oxidative effect on the L02 hepatocyte model of insulin resistance induced by high glucose/high insulin.

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Allman, K. G., A. P. Stoddart, M. M. Kennedy, and J. D. Young. "L-arginine augments nitric oxide production and mesenteric blood flow in ovine endotoxemia." American Journal of Physiology-Heart and Circulatory Physiology 271, no. 4 (October 1, 1996): H1296—H1301. http://dx.doi.org/10.1152/ajpheart.1996.271.4.h1296.

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We studied the effects of administrating the nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), or the nitric oxide precursor, L-arginine, on hemodynamic variables and serum nitrate concentrations in an anesthetized ovine model of endotoxemia to assess the effects on regional visceral blood flow and to determine whether L-arginine availability limits nitric oxide production. Animals received Escherichia coli endotoxin (2 micrograms/kg) followed 2 h later by L-NAME (25 mg/kg), L-arginine (0.575 g/kg), or saline administered over 1 h followed by an infusion of the same dose over 8 h (n = 6 per group). Renal and mesenteric blood flow were measured by placement of electromagnetic flow probes, and serum nitrate concentrations were determined using vanadium III chloride or nitrate reductase reduction to nitric oxide or nitrite, respectively. The results showed L-NAME significantly increased systemic vascular resistance (P < 0.01), decreased serum nitrate concentrations (P < 0.05), and caused a transient reduction in mesenteric blood flow (P < 0.05). L-Arginine caused a reduction in systemic vascular resistance (P < 0.01), increased mesenteric blood flow (P < 0.001) and conductance (P < 0.05). There were no significant changes in renal arterial blood flow in either group. We conclude that the availability of L-arginine limits nitric oxide production in endotoxemia and, furthermore, that L-arginine administration in this model causes significant mesenteric vasodilatation. L-NAME administration had only limited effect on visceral blood flow despite a marked increase in systemic vascular resistance and a reduction in nitric oxide production.

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Ryan, Jeremy, Garry Jennings, Frank Dudley, and Jaye Chin-Dusting. "Smooth Muscle-Derived Nitric Oxide is Elevated in Isolated Forearm Veins in Human Alcoholic Cirrhosis." Clinical Science 91, no. 1 (July 1, 1996): 23–28. http://dx.doi.org/10.1042/cs0910023.

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1. Cirrhosis is often complicated by disturbances in the systemic circulation. We have previously demonstrated decreased vascular responses to vasoconstrictors in forearm resistance arteries in subjects with alcoholic cirrhosis. In the current study we investigate the role of the potent endogenous vasodilator nitric oxide in the peripheral circulation of these patients. 2. Ten patients with alcoholic cirrhosis (Pugh grade A) and 10 age-matched control subjects were studied. The effect of blockade of nitric oxide synthesis was studied both in vivo in forearm resistance arteries using forearm venous occlusion plethysmography and in vitro in veins isolated from the forearm. The role of endothelium-derived nitric oxide was studied in vivo using the endothelium-dependent vasodilator acetylcholine. 3. Mean arterial pressure and forearm basal flow in vivo were similar in the two groups. The constrictor response (percentage decrease in forearm blood flow) to noradrenaline (100 ng/min) was 26% smaller in patients with cirrhosis (31.65 ± 2.64%) than in control subjects (42.75 ± 3.87%, P = 0.037). Constrictor responses to the nitric oxide synthase inhibitor NG-monomethyl-l-arginine were not different in the two groups. Dilator responses to acetylcholine were significantly attenuated in cirrhotic patients compared with control subjects. 4. To investigate the role of smooth muscle-derived nitric oxide in vitro, all veins were stripped of their endothelium. Responses to noradrenaline were significantly diminished in veins isolated from patients with cirrhosis compared with control subjects. Incubation with the nitric oxide synthase inhibitor Nω-nitro-l-arginine had no effect on responses to noradrenaline in veins from control subjects but significantly enhanced the maximal response to noradrenaline by 23.95% (range 3.77–100%, P = 0.043) in veins from patients with cirrhosis. 5. Responses to noradrenaline were attenuated in vivo in forearm resistance arteries in patients with alcoholic cirrhosis. This impairment was also apparent in forearm isolated veins, stripped of the endothelium. Our data exclude a major role for endothelium-derived nitric oxide but highlight a possible role for smooth muscle-derived nitric oxide.

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Clement, M. G., and M. Dimori. "Inhaled Nitric Oxide Counterbalances ET-1 Dependent Pulmonary Hypertension and Bronchoconstriction in the Pig." Mediators of Inflammation 3, no. 2 (1994): 131–35. http://dx.doi.org/10.1155/s0962935194000165.

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In anaesthetized, paralysed, ventilated pigs the ability of inhaled nitric oxide (80 ppm in 02) to reduce the haemodynamic and respiratory effects of endothelin-1 administration (200 pmol/kg, i.v.) was evaluated. The mechanical properties of the respiratory system were evaluated by the rapid airway occlusion technique. The overall respiratory resistance, the interrupter resistance and the additional resistance that reflects the viscoelastic properties of tissues and the inequality of the time constant within the system were also evaluated. The results show that inhaled nitric oxide can act as a selective pulmonary vasodilator and as a bronchodilator to counteract the vasoconstrictor and bronchoconstrictor activity of endothelin-1. In the pig, nitric oxide inhaled at 80 ppm for 6 mitt reduced the changes in respiratory-, interrupter- and additional resistance due to endothelin-1 administration without significantly changing the static and dynamic elastance of the respiratory system.

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Miloradovic, Zoran, Maja Gvozdenov, Djurdjica Jovovic, Nevena Mihailovic-Stanojevic, Milan Ivanov, Una Vajic, Danijela Karanovic, Sladjan Milanovic, and Jelica Grujic-Milanovic. "Effect of Olea europea L. leaf extract on haemodynamic status and lipid peroxidation in spontaneously hypertensive rats." Veterinarski glasnik 67, no. 5-6 (2013): 303–15. http://dx.doi.org/10.2298/vetgl1306303m.

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Hypertension is one of the main causes of cardiovascular disorders and since ancient times olive tree leaves have been used in its therapy. However the mechanisms of their atihypertensive effect have not been sufficiently explained yet. The main objective of our study was to investigate acute effect of olive tree leaves extract on haemodynamics and lipid peroxidation in rats with congenital hypertension under normal and blocked synthesis of nitric oxide. For the purpose of our research, there were used olive tree leaf extract EFLA? 943 as well as inhibitor of nitric oxide synthase enzyme L-NAME. Nitric oxide synthesis inhibition led to statistically significant increase of mean arterial pressure, reducing heart rate and cardiac output, increase of total vascular resistance and lipid peroxidation in plasma. Treatment by olive leaf extract led to decrease of mean arterial pressure, reducing the frequency and cardiac output, without change in lipid peroxidation. Olive leaf extract under blockade of nitric oxide led to decrease of mean arterial pressure, total peripheral resistance remained high, cardiac output low, and lipid peroxidation significantly increased. General conclusion is that olive leaf extract has a strong antihypertensive effect, decreases cardiac pre and after load and does not influence lipid peroxidation. Under blockade of nitric oxide synthesis, this extract keeps antihypertensive properties, but due to strong endothelial dysfunction, it is unable to regulate increased total peripheral resistance and marked lipid peroxidation.

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Sladek, S. M., R. R. Magness, and K. P. Conrad. "Nitric oxide and pregnancy." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 272, no. 2 (February 1, 1997): R441—R463. http://dx.doi.org/10.1152/ajpregu.1997.272.2.r441.

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This review will consider whether nitric oxide (NO) contributes to maternal systemic vasodilation during pregnancy, regulates uterine and fetoplacental blood flow, and is involved in uterine quiescence prior to parturition. Also, whether a deficiency of NO contributes to the hypertensive disorder of pregnancy, preeclampsia, will be considered. The biosynthesis of NO increases in gravid rats and sheep, but the status in normal human pregnancy and preeclampsia is controversial. NO contributes to maternal systemic vasodilation and reduced vascular reactivity during normal pregnancy; however, the relative contribution of NO is variable depending on the animal species, vascular bed, and vessel size. Impaired relaxation responses to acetylcholine, but not bradykinin or NO donors, are observed in small arteries from women with preeclampsia, suggesting a receptor or signal transduction defect, although NO may play little, if any, role here. Uterine arteries have increased endothelial nitric oxide synthase (NOS) activity, protein expression, and guanosine 3',5'-cyclic monophosphate production during pregnancy; however, whether these mediate uterine vasodilation during pregnancy remains to be established. NOS is expressed in the human placental syncytiotrophoblast and in the fetoplacental and umbilical vascular endothelium where basal production of NO contributes to low fetoplacental vascular resistance. Controversy exists over the status of placental NOS in preeclampsia, although an abnormality of umbilical NOS activity is likely. Finally, the uterus has NOS activity, which decreases at the end of gestation, and exogenous NO relaxes the myometrium, but whether endogenous NO contributes to uterine quiescence during pregnancy has yet to be confirmed.

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Mayhan, William G., and Denise M. Arrick. "Tetrahydrobiopterin rescues impaired responses of cerebral resistance arterioles during type 1 diabetes." Diabetes and Vascular Disease Research 14, no. 1 (November 14, 2016): 33–39. http://dx.doi.org/10.1177/1479164116675490.

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Our goal was to test the hypothesis that administration of tetrahydrobiopterin (BH4) would improve impaired endothelial nitric oxide synthase–dependent dilation of cerebral arterioles during type 1 diabetes. In addition, we examined the influence of BH4 on levels of superoxide in brain tissue. In vivo diameter of cerebral arterioles in nondiabetic and diabetic rats was measured in response to endothelial nitric oxide synthase–dependent agonists (acetylcholine and adenosine 5′-diphosphate) and an endothelial nitric oxide synthase–independent agonist (nitroglycerine) before and during application of BH4 (1.0 µM). We also measured levels of superoxide from cortex tissue in nondiabetic and diabetic rats under basal states and during BH4. Acetylcholine and adenosine 5′-diphosphate dilated cerebral arterioles in nondiabetic rats, but this vasodilation was significantly impaired in diabetic rats. In contrast, nitroglycerine produced similar vasodilation in nondiabetic and diabetic rats. Application of BH4 did not enhance vasodilation in nondiabetic rats but improved impaired cerebral vasodilation in diabetic rats. Basal superoxide levels were increased in cortex tissue from diabetic rats, and BH4 reduced these levels to that found in nondiabetic rats. Thus, BH4 is an important mediator of endothelial nitric oxide synthase–dependent responses of cerebral arterioles in diabetes and may have therapeutic potential for the treatment of cerebral vascular disease.

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Kovalyova, O. M., G. V. Demydenko, and T. M. Ambrosova. "THERAPEUTIC POTENTIAL OF METFORMIN: INFLUENCE ON CARBOHYDRATE METABOLISM AND VASOACTIVE NITRIC OXIDE POOL IN PATIENTS WITH COMORBID PATHOLOGY." Problems of Endocrine Pathology 42, no. 4 (December 25, 2012): 57–64. http://dx.doi.org/10.21856/j-pep.2012.4.09.

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It studied the metformin action on vasoactive nitric oxide pool in patients with essential hypertension with accompanied type 2 diabetes mellitus. Treatment with metformin during 3 months caused positive influence on vasoactive nitric oxide pool in patients with essential hypertension with accompanied type 2 diabetes mellitus. Pharmacologic effects of metformin connect with increasing of endothelial nitric oxide synthase, decreasing if inducible nitric oxide synthase, glicemic control, diminishing of insulin, glicated hemoglobin and insulin resistance indexes. Metformin as a first choice medicine for the patients with essential hypertension and type 2 diabetes mellitus doesn’t cause and complication that leads to the cancelling of the treatment.

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Sinha, Birandra K., Lalith Perera, and Ronald E. Cannon. "NCX-4040, a Unique Nitric Oxide Donor, Induces Reversal of Drug-Resistance in Both ABCB1- and ABCG2-Expressing Multidrug Human Cancer Cells." Cancers 13, no. 7 (April 2, 2021): 1680. http://dx.doi.org/10.3390/cancers13071680.

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The emergence of multidrug resistance (MDR) in the clinic is a significant problem for a successful treatment of human cancers. Overexpression of various ABC transporters (P-gp, BCRP and MRP’s), which remove anticancer drugs in an ATP-dependent manner, is linked to the emergence of MDR. Attempts to modulate MDR have not been very successful in the clinic. Furthermore, no single agent has been found to significantly inhibit their functions to overcome clinical drug resistance. We have previously shown that nitric oxide (●NO) inhibits ATPase functions of ABC transporters, causing reversal of resistance to clinically active anticancer drugs. In this study, we have used cytotoxicity and molecular docking studies to show that NCX4040, a nitric oxide donor related to aspirin, inhibited the functions of ATPase which resulted in significant reversal of resistance to both adriamycin and topotecan in P-gp- and BCRP-expressing human cancer cell lines, respectively. We also used several other cytotoxic nitric oxide donors, e.g., molsidomine and S-nitroso glutathione; however, both P-gp- and BCRP-expressing cells were found to be highly resistant to these NO-donors. Molecular docking studies showed that NCX4040 binds to the nucleotide binding domains of the ATPase and interferes with further binding of ATP, resulting in decreased activities of these transporters. Our results are extremely promising and suggest that nitric oxide and other reactive species delivered to drug resistant tumor cells by well-designed nitric oxide donors could be useful in sensitizing anticancer drugs in multidrug resistant tumors expressing various ABC transporters.

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Fahey, Jonathan, and Albert Girotti. "Nitric Oxide Antagonism to Anti-Glioblastoma Photodynamic Therapy: Mitigation by Inhibitors of Nitric Oxide Generation." Cancers 11, no. 2 (February 15, 2019): 231. http://dx.doi.org/10.3390/cancers11020231.

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Many studies have shown that low flux nitric oxide (NO) produced by inducible NO synthase (iNOS/NOS2) in various tumors, including glioblastomas, can promote angiogenesis, cell proliferation, and migration/invasion. Minimally invasive, site-specific photodynamic therapy (PDT) is a highly promising anti-glioblastoma modality. Recent research in the authors’ laboratory has revealed that iNOS-derived NO in glioblastoma cells elicits resistance to 5-aminolevulinic acid (ALA)-based PDT, and moreover endows PDT-surviving cells with greater proliferation and migration/invasion aggressiveness. In this contribution, we discuss iNOS/NO antagonism to glioblastoma PDT and how this can be overcome by judicious use of pharmacologic inhibitors of iNOS activity or transcription.

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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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Xu, X. P., J. S. Pollock, M. A. Tanner, and P. R. Myers. "Hypoxia activates nitric oxide synthase and stimulates nitric oxide production in porcine coronary resistance arteriolar endothelial cells." Cardiovascular Research 30, no. 6 (December 1, 1995): 841–47. http://dx.doi.org/10.1016/s0008-6363(95)00117-4.

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XU, X. "Hypoxia activates nitric oxide synthase and stimulates nitric oxide production in porcine coronary resistance arteriolar endothelial cells." Cardiovascular Research 30, no. 6 (December 1995): 841–47. http://dx.doi.org/10.1016/0008-6363(95)00117-4.

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Su, Zhanhai, Jürgen Kuball, Ana-Paula Barreiros, Daniela Gottfried, Edite Antunes Ferreira, Matthias Theobald, Peter R. Galle, Dennis Strand, and Susanne Strand. "Nitric Oxide Promotes Resistance to Tumor Suppression by CTLs." Journal of Immunology 176, no. 7 (March 17, 2006): 3923–30. http://dx.doi.org/10.4049/jimmunol.176.7.3923.

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Journal articles on the topic 'Nitric oxide resistance'

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