Hydrogen Peroxide‐Induced Broncho‐ and Vasoconstriction in the Isolated Perfused and Ventilated Guinea Pig Lung

Bannenberg, Gerard; Kimland, Monika; Ryrfeldt, Åke; Moldéus, Peter

doi:10.1111/j.1600-0773.1993.tb01657.x

Cited by 19 publications

(12 citation statements)

References 34 publications

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“…Expression of iNOS was increased in the pulmonary vessels, and the associated increase in NO concentration is evident in part by the elevated SNO levels. Proteins with cysteine(s) modified to SNO potentially provide a stable pool of bioactive NO adducts mediating some biologic activity of endogenous NO, regulating airway and pulmonary artery tone (31)(32)(33). Rats exposed to Ͼ95% oxygen, however, had a decrease in SNO in BAL and tissue.…”

Section: Discussionmentioning

confidence: 99%

Oxygen Tension and Inhaled Nitric Oxide Modulate Pulmonary Levels of S-Nitrosocysteine and 3-Nitrotyrosine in Rats

et al. 2004

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The oxidative environment within the lung generated upon administration of oxygen may be a critical regulator for the efficacy of inhaled nitric oxide therapy, possibly as a consequence of changes in nitrosative and nitrative chemistry. Changes in S-nitrosocysteine and 3-nitrotyrosine adducts were therefore evaluated after exposure of rats to 80% or Ͼ95% oxygen for 24 or 48 h with and without 20 ppm inhaled nitric oxide. Exposure to 80% oxygen led to increased formation of S-nitrosocysteine and 3-nitrotyrosine adducts in lung tissue that were also associated with increased expression of iNOS. The addition of inhaled nitric oxide in 80% oxygen exposure did not alter any of these adducts in the lung or in the bronchoalveolar lavage (BAL). Exposure to Ͼ95% oxygen led to a significant decrease in S-nitrosocysteine and an increase in 3-nitrotyrosine adducts in the lung. Co-administration of inhaled nitric oxide with Ͼ95% oxygen prevented the decrease in S-nitrosocysteine levels. The levels of S-nitrosocysteine and 3-nitrotyrosine returned to baseline in a time-dependent fashion after termination of exposure to Ͼ95% oxygen and inhaled nitric oxide. These data suggest the formation of S-nitrosating and tyrosine-nitrating species is regulated by oxygen tensions and co-administration of inhaled nitric oxide restores the nitrosative chemistry without a significant impact upon the nitrative pathway. (1-4). The use of inhaled NO has been shown to improve oxygenation in premature infants with severe hypoxemic respiratory failure (5), and a preliminary study of infants with established CLD has shown both a reduced supplemental oxygen requirement and improved arterial oxygen tension in 11 of 16 infants (6). More recently, Schreiber et al. (7) have demonstrated a decrease in death and chronic lung disease in premature infants given inhaled NO.One of the concerns regarding the use of inhaled NO in conjunction with hyperoxia has been the potential of forming secondary reactive nitrogen species (8 -10). Hyperoxia induces the formation of reactive oxygen species, which may consume NO, preventing its therapeutic effects. The reactive nitrogen species formed may also contribute to oxidative injury, and evidence for protein oxidation and nitration has been accumulating in experimental models of hyperoxia-induced lung injury. In particular, hyperoxia has been found to cause damage to alveolar epithelium and endothelium (11,12), and extensive nitration in airway epithelium and alveolar interstitium has been noted in female mice exposed to hyperoxia (13). Recently, in a model of hyperoxia in newborn rats, macrophages were demonstrated to play a significant role in the generation of reactive oxygen species and 3-nitrotyrosine (14). Peroxidases may also contribute to the formation of nitrative species (15, 16), and myeloperoxidase specifically has been implicated

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Section: Discussionmentioning

confidence: 99%

Oxygen Tension and Inhaled Nitric Oxide Modulate Pulmonary Levels of S-Nitrosocysteine and 3-Nitrotyrosine in Rats

et al. 2004

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“…Interestingly, there is increasing evidence for another mechanism, in addition to guanylyl cyclase activation, by which NO relaxes human bronchial smooth muscle (24,127,199,341,421). One of the metabolic pathways for NO also involves its reaction in the presence of thiol to form SNOs (126).…”

Section: No and Airway Smooth Muscle Relaxationmentioning

confidence: 99%

Nitric Oxide in Health and Disease of the Respiratory System

Ricciardolo¹,

Sterk²,

Gaston³

et al. 2004

Physiological Reviews

793

649

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During the past decade a plethora of studies have unravelled the multiple roles of nitric oxide (NO) in airway physiology and pathophysiology. In the respiratory tract, NO is produced by a wide variety of cell types and is generated via oxidation of l-arginine that is catalyzed by the enzyme NO synthase (NOS). NOS exists in three distinct isoforms: neuronal NOS (nNOS), inducible NOS (iNOS), and endothelial NOS (eNOS). NO derived from the constitutive isoforms of NOS (nNOS and eNOS) and other NO-adduct molecules (nitrosothiols) have been shown to be modulators of bronchomotor tone. On the other hand, NO derived from iNOS seems to be a proinflammatory mediator with immunomodulatory effects. The concentration of this molecule in exhaled air is abnormal in activated states of different inflammatory airway diseases, and its monitoring is potentially a major advance in the management of, e.g., asthma. Finally, the production of NO under oxidative stress conditions secondarily generates strong oxidizing agents (reactive nitrogen species) that may modulate the development of chronic inflammatory airway diseases and/or amplify the inflammatory response. The fundamental mechanisms driving the altered NO bioactivity under pathological conditions still need to be fully clarified, because their regulation provides a novel target in the prevention and treatment of chronic inflammatory diseases of the airways.

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“…To confirm the RDA results, we used sublethal doses of a series of additional NO donors and a human MC line to verify the universality of changes in gene expression elicited by GSNO treatment (Bannenberg et al, 1995) in rat MCs. Human MCs were conditioned to maintain amplified levels of matrix-associated genes and proteins by treatment with TGF-b and high levels of glucose, thus mimicking a fibrotic environment.…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide modulates expression of extracellular matrix genes linked to fibrosis in kidney mesangial cells

Wani

Carl²,

Henger³

et al. 2007

BCHM

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Mesangial cells are thought to be important mediators of glomerular inflammation and fibrosis. Studies have established a direct role for nitric oxide (NO) in the regulation of gene expression in mesangial cells. Representational difference analysis was used to investigate changes in gene expression elicited by the treatment of S-nitroso-L-glutathione in rat mesangial cells. Seven upregulated and 11 downregulated genes were identified. Four out of 11 downregulated genes (connective tissue growth factor, thrombospondin-1, collagen type I a1 and collagen type I a2) are known to be linked to inflammation and fibrosis. Results were verified across species in mesangial cells treated with a series of NO donors using Northern blot analysis, quantitative real-time PCR and protein analysis methods. Induction of endogenous NO production by cytokine stimulation also triggered regulation of the genes. One example gene, connective tissue growth factor, was studied at the promoter level. Promoter-reporter gene studies in mesangial cells demonstrated that NO acts at the transcriptional level to suppress gene expression. Our results reveal a complex role of NO in regulating gene expression in mesangial cells and suggest an antifibrotic potential for NO.

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Hydrogen Peroxide‐Induced Broncho‐ and Vasoconstriction in the Isolated Perfused and Ventilated Guinea Pig Lung

Cited by 19 publications

References 34 publications

Oxygen Tension and Inhaled Nitric Oxide Modulate Pulmonary Levels of S-Nitrosocysteine and 3-Nitrotyrosine in Rats

Oxygen Tension and Inhaled Nitric Oxide Modulate Pulmonary Levels of S-Nitrosocysteine and 3-Nitrotyrosine in Rats

Nitric Oxide in Health and Disease of the Respiratory System

Nitric oxide modulates expression of extracellular matrix genes linked to fibrosis in kidney mesangial cells

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