The dual personality of NO

Colasanti, Marco; Suzuki, Hisanori

doi:10.1016/s0165-6147(00)01499-1

Cited by 337 publications

(252 citation statements)

References 18 publications

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“…The ESW-induced enhancement of constitutive NOS-dependent NO levels is worth of interest when we take into account the recent notion that physiological, low levels of NO, similar to those produced by the basal activity of nNOS and/or eNOS, prevent induction of iNOS mRNA expression (but also of other NF-jB-dependent genes, including TNF-a and cyclooxygenase-2) through the suppression of NF-jB activation [17,[19][20][21][22][23]. As a consequence, iNOS gene expression takes place after LPS/cytokine stimulation, provided that the cNOS-generated NO is reduced below a threshold value in a short time [15,17].…”

Section: Resultsmentioning

confidence: 99%

Nitric oxide mediates anti‐inflammatory action of extracorporeal shock waves

et al. 2005

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Here, we show that extracorporeal shock waves (ESW), at a low energy density value, quickly increase neuronal nitric oxide synthase (nNOS) activity and basal nitric oxide (NO) production in the rat glioma cell line C6. In addition, the treatment of C6 cells with ESW reverts the decrease of nNOS activity and NO production induced by a mixture of lipopolysaccharides (LPS), interferon-c (IFN-c) plus tumour necrosis factor-a (TNF-a). Finally, ESW treatment efficiently downregulates NF-jB activation and NF-jB-dependent gene expression, including inducible NOS and TNF-a. The present report suggests a possible molecular mechanism of the anti-inflammatory action of ESW treatment.

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Section: Resultsmentioning

confidence: 99%

Nitric oxide mediates anti‐inflammatory action of extracorporeal shock waves

et al. 2005

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“…Nitric oxide is capable of inhibiting neutrophil superoxide anion production via a direct action on the membrane components of NADPH oxidase and the assembly of NADH/NADPH oxidase subunits [25]. However, NO has been considered to be a double-edged sword [26,27]. It is well known that NO in the presence of superoxide can form the toxic peroxynitrite.…”

Section: Discussionmentioning

confidence: 99%

Tissue kallikrein infusion prevents cardiomyocyte apoptosis, inflammation and ventricular remodeling after myocardial infarction

Yao

Yin

Shen

et al. 2007

Regulatory Peptides

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We investigated the effect of tissue kallikrein infusion on cardiac protection at acute and sub-acute phases after myocardial infarction (MI). Immediately after MI, rats were infused with purified tissue kallikrein, with or without icatibant (a kinin B2 receptor antagonist). Intramyocardial injection of kallikrein reduced myocardial infarct size and inhibited cardiomyocyte apoptosis at 1 day after MI associated with increased nitric oxide levels, Akt and glycogen synthase kinase-3β phosphorylation and decreased caspase-3 activation. Kallikrein infusion for 7 days improved cardiac function, normalized left ventricular wall thickness and decreased monocyte/macrophage infiltration in the infarct heart. Kallikrein treatment reduced NADH oxidase expression and activity, superoxide formation and malondialdehyde levels, and reduced MAPK and Iκ-Bα phosphorylation, NF-κB activation and MCP-1 and VCAM-1 expression. Kallikrein's effects were all blocked by icatibant. These results indicate that kallikrein through kinin B2 receptor activation prevents apoptosis, inflammation and ventricular remodeling by increased nitric oxide formation and suppression of oxidative stress-mediated signaling pathways.

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“…Haddad et al (1995) demonstrated an increase in iNOS mRNA expression at 2 and 8 h after ozone exposure of Brown Norway rats. Interestingly, Colasanti & Suzuki (2000) suggest that basal levels of NO suppress NF-kB dissociation from the inhibitory nuclear transcription factor (I-kB) complex and also prevent NF-kB binding to the promoter region of the iNOS gene. Thus, in the present study, the initial NO-de®ciency during the ozone-induced EPB, could facilitate activation of the machinery to up-regulate iNOS expression during the LBP.…”

Section: Discussionmentioning

confidence: 99%

“…Derived from the nitric oxide synthase (NOS) conversion of L-arginine to L-citrulline, a basal level of the free radical, NO, maintains bronchodilatory airway tone, suppresses leukocyte activation and inhibits microvascular leakage (Barnes et al, 1999;Colasanti & Suzuki, 2000). However, excess airways NO, although having bene®cial anti-bacterial and anti-viral activity, increases microvascular permeability to cause pulmonary oedema and promotes leukocyte in¯ux and adhesion in the airways (Barnes et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Airway function, oedema, cell infiltration and nitric oxide generation in conscious ozone‐exposed guinea‐pigs: effects of dexamethasone and rolipram

Toward

Broadley

2002

British J Pharmacology

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1 The e ects of ozone inhalation (90 min, 2.15+0.05 p.p.m.) and their modi®cation by dexamethasone (20 mg kg 71 ) or the phosphodiesterase-4 inhibitor, rolipram (1 mg kg 71 ), administered (i.p.) 24 and 0.5 h before and 24 h after ozone exposure were examined in conscious guineapigs. 2 Ozone caused an early-phase bronchoconstriction (EPB) as a fall in speci®c airways conductance (sG aw ) measured by whole body plethysmography, followed at 5 h by a late-phase bronchoconstriction (LPB) and increased respiratory rate. Rolipram did not alter this pro®le but dexamethasone inhibited the EPB. 3 Airway hyperreactivity to inhaled histamine (1 mM, 20 s) occurred at 0.5, 2, 12, 24 and 48 h after ozone inhalation, the 2 h change being abolished by rolipram and dexamethasone. 4 Bronchoalveolar lavage¯uid (BALF) macrophages, eosinophils and neutrophils were signi®cantly (P50.05) elevated at 12, 24 and 48 h after ozone exposure, the 48 h in¯ux being signi®cantly attenuated (P50.05) by rolipram and dexamethasone. 5 BALF nitric oxide (NO) metabolites decreased 0.5 h after ozone exposure by 52%, recovered at 2 h and signi®cantly increased at 12 (101%) and 24 h (127%). The elevated NO was una ected by rolipram or dexamethasone. 6 Lung oedema, measured from wet/dry weight di erences, was signi®cant 12, 24 and 48 h after ozone exposure, the latter being signi®cantly attenuated (P50.05) by rolipram and dexamethasone. 7 Ozone exposure of guinea-pigs produced features common to COPD. Although rolipram and dexamethasone did not a ect the airway function changes, they inhibited the in¯ammation, airway hyperreactivity and oedema.

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The dual personality of NO

Cited by 337 publications

References 18 publications

Nitric oxide mediates anti‐inflammatory action of extracorporeal shock waves

Nitric oxide mediates anti‐inflammatory action of extracorporeal shock waves

Tissue kallikrein infusion prevents cardiomyocyte apoptosis, inflammation and ventricular remodeling after myocardial infarction

Airway function, oedema, cell infiltration and nitric oxide generation in conscious ozone‐exposed guinea‐pigs: effects of dexamethasone and rolipram

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