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Article: Regulation of murine airway responsiveness by endothelial nitric oxide synthase

TitleRegulation of murine airway responsiveness by endothelial nitric oxide synthase
Authors
Issue Date2001
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajplung.physiology.org/
Citation
American Journal Of Physiology - Lung Cellular And Molecular Physiology, 2001, v. 281 n. 1 25-1, p. L258-L267 How to Cite?
AbstractNitric oxide (NO) is a potent vasodilator, but it can also modulate contractile responses of the airway smooth muscle. Whether or not endothelial (e) NO synthase (NOS) contributes to the regulation of bronchial tone is unknown at present. Experiments were designed to investigate the isoforms of NOS that are expressed in murine airways and to determine whether or not the endogenous release of NO modulates bronchial tone in wild-type mice and in mice with targeted deletion of eNOS [eNOS(-/-)]. The presence of neuronal NOS (nNOS), inducible NOS (iNOS), and eNOS in murine trachea and lung parenchyma was assessed by RT-PCR, immunoblotting, and immunohistochemistry. Airway resistance was measured in conscious unrestrained mice by means of a whole body plethysmography chamber. The three isoforms of NOS were constitutively present in lungs of wild-type mice, whereas only iNOS and nNOS were present in eNOS(-/-) mice. Labeling of nNOS was localized in submucosal airway nerves but was not consistently detected, and iNOS immunoreactivity was observed in tracheal and bronchiolar epithelial cells, whereas eNOS was expressed in endothelial cells. In wild-type mice, treatment with N-nitro-L-arginine methyl ester, but not with aminoguanidine, potentiated the increase in airway resistance produced by inhalation of methacholine. eNOS(-/-) mice were hyperresponsive to inhaled methacholine and markedly less sensitive to N-nitro-L-arginine methyl ester. These results demonstrate that the three NOS isoforms are expressed constitutively in murine lung and that NO derived from eNOS plays a physiological role in controlling bronchial airway reactivity.
Persistent Identifierhttp://hdl.handle.net/10722/171256
ISSN
2015 Impact Factor: 4.721
2015 SCImago Journal Rankings: 1.838
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFeletou, Men_US
dc.contributor.authorLonchampt, Men_US
dc.contributor.authorCoge, Fen_US
dc.contributor.authorGalizzi, JPen_US
dc.contributor.authorBassoullet, Cen_US
dc.contributor.authorMerial, Cen_US
dc.contributor.authorRobineau, Pen_US
dc.contributor.authorBoutin, JAen_US
dc.contributor.authorHuang, PLen_US
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorCanet, Een_US
dc.date.accessioned2012-10-30T06:12:59Z-
dc.date.available2012-10-30T06:12:59Z-
dc.date.issued2001en_US
dc.identifier.citationAmerican Journal Of Physiology - Lung Cellular And Molecular Physiology, 2001, v. 281 n. 1 25-1, p. L258-L267en_US
dc.identifier.issn1040-0605en_US
dc.identifier.urihttp://hdl.handle.net/10722/171256-
dc.description.abstractNitric oxide (NO) is a potent vasodilator, but it can also modulate contractile responses of the airway smooth muscle. Whether or not endothelial (e) NO synthase (NOS) contributes to the regulation of bronchial tone is unknown at present. Experiments were designed to investigate the isoforms of NOS that are expressed in murine airways and to determine whether or not the endogenous release of NO modulates bronchial tone in wild-type mice and in mice with targeted deletion of eNOS [eNOS(-/-)]. The presence of neuronal NOS (nNOS), inducible NOS (iNOS), and eNOS in murine trachea and lung parenchyma was assessed by RT-PCR, immunoblotting, and immunohistochemistry. Airway resistance was measured in conscious unrestrained mice by means of a whole body plethysmography chamber. The three isoforms of NOS were constitutively present in lungs of wild-type mice, whereas only iNOS and nNOS were present in eNOS(-/-) mice. Labeling of nNOS was localized in submucosal airway nerves but was not consistently detected, and iNOS immunoreactivity was observed in tracheal and bronchiolar epithelial cells, whereas eNOS was expressed in endothelial cells. In wild-type mice, treatment with N-nitro-L-arginine methyl ester, but not with aminoguanidine, potentiated the increase in airway resistance produced by inhalation of methacholine. eNOS(-/-) mice were hyperresponsive to inhaled methacholine and markedly less sensitive to N-nitro-L-arginine methyl ester. These results demonstrate that the three NOS isoforms are expressed constitutively in murine lung and that NO derived from eNOS plays a physiological role in controlling bronchial airway reactivity.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajplung.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Lung Cellular and Molecular Physiologyen_US
dc.subject.meshAirway Resistance - Drug Effects - Physiologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBrain - Metabolismen_US
dc.subject.meshBronchi - Drug Effects - Physiologyen_US
dc.subject.meshCholinergic Agonists - Pharmacologyen_US
dc.subject.meshLung - Drug Effects - Metabolismen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred Strainsen_US
dc.subject.meshMice, Knockout - Geneticsen_US
dc.subject.meshNitric Oxide Synthase - Genetics - Physiologyen_US
dc.subject.meshNitric Oxide Synthase Type Ien_US
dc.subject.meshNitric Oxide Synthase Type Iien_US
dc.subject.meshNitric Oxide Synthase Type Iiien_US
dc.subject.meshRna, Messenger - Metabolismen_US
dc.subject.meshReference Valuesen_US
dc.subject.meshTrachea - Drug Effects - Metabolismen_US
dc.titleRegulation of murine airway responsiveness by endothelial nitric oxide synthaseen_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid11404269-
dc.identifier.scopuseid_2-s2.0-0034815869en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034815869&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume281en_US
dc.identifier.issue1 25-1en_US
dc.identifier.spageL258en_US
dc.identifier.epageL267en_US
dc.identifier.isiWOS:000169546800032-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridFeletou, M=7006461826en_US
dc.identifier.scopusauthoridLonchampt, M=7003363063en_US
dc.identifier.scopusauthoridCoge, F=6602987151en_US
dc.identifier.scopusauthoridGalizzi, JP=7004145226en_US
dc.identifier.scopusauthoridBassoullet, C=14067038300en_US
dc.identifier.scopusauthoridMerial, C=6506139794en_US
dc.identifier.scopusauthoridRobineau, P=55041561100en_US
dc.identifier.scopusauthoridBoutin, JA=7102994898en_US
dc.identifier.scopusauthoridHuang, PL=7403659318en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridCanet, E=7006072145en_US

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