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Article: Augmentation of hypoxia-induced nitric oxide generation in the rat carotid body adapted to chronic hypoxia: An involvement of constitutive and inducible nitric oxide synthases

TitleAugmentation of hypoxia-induced nitric oxide generation in the rat carotid body adapted to chronic hypoxia: An involvement of constitutive and inducible nitric oxide synthases
Authors
KeywordsCarotid body
Chemoreceptor
Chronic hypoxia
L-NAME
Nitric oxide
Nitric oxide synthase
Issue Date2002
PublisherSpringer. The Journal's web site is located at http://link.springer.de/link/service/journals/00424/index.htm
Citation
Pflugers Archiv European Journal Of Physiology, 2002, v. 444 n. 1-2, p. 178-185 How to Cite?
AbstractAcute hypoxia increases the endogenous release of nitric oxide (NO) in rat carotid body and the expression of nitric oxide synthases is modulated by chronic hypoxia. The aim of the study was to examine hypoxia-induced NO generation in rat carotid body adapted to chronic hypoxia with inspired oxygen at 10% for 4 weeks. The concentration of NO was measured electrochemically with a Pt/Nafion/Pd-IrOx/POAP modified electrode inserted into the isolated carotid body superfused with bicarbonate-buffer saline at 35°C. Acute hypoxia increased the concentration of NO by 471.3±71.4 nM in the carotid body of chronically hypoxic (CH) rats. The amount of NO release induced by hypoxia was significantly augmented when compared with that of the normoxic control (87.6±15.9 nM). The hypoxia-induced NO generation was markedly attenuated by pretreatment with L-NG-nitroarginine methylester (L-NAME; 500 μM), a non-selective nitric oxide synthase (NOS) inhibitor and also by removal of extracellular calcium with the calcium chelator EGTA (5 mM). Additionally, NO generation during hypoxia was reduced by 30% in the CH carotid body treated with S-methylisothiourea (SMT; 50 μM), a specific blocker of inducible NOS (iNOS). Immunohistochemical study revealed that positive iNOS protein immunoreactivity was detected in clusters of glomus cells in the carotid bodies of CH rats, but not in the normoxic group. Thus, chronic hypoxia enhances hypoxia-induced NO generation mediated by calcium-dependent NOSs and iNOS in the carotid body. Extracellular recording of sinus nerve activity of CH carotid bodies showed that L-NAME treatment enhanced the afferent discharge in response to hypoxia, confirming that the generation of NO suppresses the activities of carotid chemoreceptors. Taken together, our results suggest that hypoxia-induced NO production increases in the rat carotid body adapted to chronic hypoxia and that constitutive and inducible NOSs are involved in the NO generation. The enhancement of NO generation may play a physiological role in blunting the hypoxic chemosensitivity during chronic hypoxia.
Persistent Identifierhttp://hdl.handle.net/10722/67583
ISSN
2015 Impact Factor: 3.654
2015 SCImago Journal Rankings: 1.638
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYe, JSen_HK
dc.contributor.authorTipoe, GLen_HK
dc.contributor.authorFung, PCen_HK
dc.contributor.authorFung, MLen_HK
dc.date.accessioned2010-09-06T05:56:25Z-
dc.date.available2010-09-06T05:56:25Z-
dc.date.issued2002en_HK
dc.identifier.citationPflugers Archiv European Journal Of Physiology, 2002, v. 444 n. 1-2, p. 178-185en_HK
dc.identifier.issn0031-6768en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67583-
dc.description.abstractAcute hypoxia increases the endogenous release of nitric oxide (NO) in rat carotid body and the expression of nitric oxide synthases is modulated by chronic hypoxia. The aim of the study was to examine hypoxia-induced NO generation in rat carotid body adapted to chronic hypoxia with inspired oxygen at 10% for 4 weeks. The concentration of NO was measured electrochemically with a Pt/Nafion/Pd-IrOx/POAP modified electrode inserted into the isolated carotid body superfused with bicarbonate-buffer saline at 35°C. Acute hypoxia increased the concentration of NO by 471.3±71.4 nM in the carotid body of chronically hypoxic (CH) rats. The amount of NO release induced by hypoxia was significantly augmented when compared with that of the normoxic control (87.6±15.9 nM). The hypoxia-induced NO generation was markedly attenuated by pretreatment with L-NG-nitroarginine methylester (L-NAME; 500 μM), a non-selective nitric oxide synthase (NOS) inhibitor and also by removal of extracellular calcium with the calcium chelator EGTA (5 mM). Additionally, NO generation during hypoxia was reduced by 30% in the CH carotid body treated with S-methylisothiourea (SMT; 50 μM), a specific blocker of inducible NOS (iNOS). Immunohistochemical study revealed that positive iNOS protein immunoreactivity was detected in clusters of glomus cells in the carotid bodies of CH rats, but not in the normoxic group. Thus, chronic hypoxia enhances hypoxia-induced NO generation mediated by calcium-dependent NOSs and iNOS in the carotid body. Extracellular recording of sinus nerve activity of CH carotid bodies showed that L-NAME treatment enhanced the afferent discharge in response to hypoxia, confirming that the generation of NO suppresses the activities of carotid chemoreceptors. Taken together, our results suggest that hypoxia-induced NO production increases in the rat carotid body adapted to chronic hypoxia and that constitutive and inducible NOSs are involved in the NO generation. The enhancement of NO generation may play a physiological role in blunting the hypoxic chemosensitivity during chronic hypoxia.en_HK
dc.languageengen_HK
dc.publisherSpringer. The Journal's web site is located at http://link.springer.de/link/service/journals/00424/index.htmen_HK
dc.relation.ispartofPflugers Archiv European Journal of Physiologyen_HK
dc.subjectCarotid bodyen_HK
dc.subjectChemoreceptoren_HK
dc.subjectChronic hypoxiaen_HK
dc.subjectL-NAMEen_HK
dc.subjectNitric oxideen_HK
dc.subjectNitric oxide synthaseen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAnoxia - metabolismen_HK
dc.subject.meshCarotid Body - drug effects - metabolismen_HK
dc.subject.meshChronic Diseaseen_HK
dc.subject.meshElectrodesen_HK
dc.subject.meshElectrophysiologyen_HK
dc.subject.meshEnzyme Inhibitors - pharmacologyen_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshNG-Nitroarginine Methyl Ester - pharmacologyen_HK
dc.subject.meshNitric Oxide - metabolismen_HK
dc.subject.meshNitric Oxide Synthase - antagonists & inhibitors - metabolismen_HK
dc.subject.meshNitric Oxide Synthase Type IIen_HK
dc.subject.meshRatsen_HK
dc.subject.meshRats, Sprague-Dawleyen_HK
dc.titleAugmentation of hypoxia-induced nitric oxide generation in the rat carotid body adapted to chronic hypoxia: An involvement of constitutive and inducible nitric oxide synthasesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0031-6768&volume=444&issue=1&spage=178&epage=185&date=2002&atitle=Augmentation+of+hypoxia-induced+nitric+oxide+generation+in+the+rat+carotid+body+adapted+to+chronic+hypoxia:+an+involvement+of+constitutive+and+inducible+nitric+oxide+synthasesen_HK
dc.identifier.emailTipoe, GL: tgeorge@hkucc.hku.hken_HK
dc.identifier.emailFung, ML: fungml@hkucc.hku.hken_HK
dc.identifier.authorityTipoe, GL=rp00371en_HK
dc.identifier.authorityFung, ML=rp00433en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s00424-002-0785-1en_HK
dc.identifier.pmid11976930-
dc.identifier.scopuseid_2-s2.0-0036261303en_HK
dc.identifier.hkuros74481en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036261303&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume444en_HK
dc.identifier.issue1-2en_HK
dc.identifier.spage178en_HK
dc.identifier.epage185en_HK
dc.identifier.isiWOS:000175781400019-
dc.publisher.placeGermanyen_HK
dc.identifier.scopusauthoridYe, JS=7403237793en_HK
dc.identifier.scopusauthoridTipoe, GL=7003550610en_HK
dc.identifier.scopusauthoridFung, PC=7101613315en_HK
dc.identifier.scopusauthoridFung, ML=7101955092en_HK

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