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Article: Acute hypoxia elevates nitric oxide generation in rat carotid body in vitro

TitleAcute hypoxia elevates nitric oxide generation in rat carotid body in vitro
Authors
Issue Date2001
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, 2001, v. 442 n. 6, p. 903-909 How to Cite?
AbstractIn acute hypoxia, the release of nitric oxide (NO) produced in rat carotid body is unclear. The concentration of NO was measured electrochemically with a Pt/Nafion/Pd-IrOx/POAP-modified electrode placed on the surface of isolated carotid bodies superfused with bicarbonate-buffer saline at 35°C. In hypoxia, the concentration of NO in the carotid body was increased by 17±2 nM. The amount of NO release during hypoxia was augmented by increasing the number of carotid bodies surrounding the electrode and also in the presence of L-arginine. In addition, the hypoxia-induced elevation of NO was abolished by pretreatment with a nitric oxide synthase (NOS) inhibitor, L-NG-nitroarginine methylester (L-NAME). The results suggest that endogenous NO production in the carotid body increases during hypoxia. Electrophysiological measurement of single fiber activity in the sinus nerve revealed that L-NAME treatment enhances the afferent discharge in response to hypoxia. This confirms that the hypoxia-induced elevation of NO suppresses the carotid chemoreceptor response to hypoxia. Taken together, it is concluded that acute hypoxia increases NO generation in the rat carotid body, and that the elevated levels of NO suppress carotid chemoreceptor activity during hypoxia. Hence, NO may play an active inhibitory role in the control of carotid chemoreceptor activity during hypoxia.
Persistent Identifierhttp://hdl.handle.net/10722/171689
ISSN
2015 Impact Factor: 3.654
2015 SCImago Journal Rankings: 1.638
References

 

DC FieldValueLanguage
dc.contributor.authorFung, MLen_US
dc.contributor.authorYe, JSen_US
dc.contributor.authorFung, PCWen_US
dc.date.accessioned2012-10-30T06:16:23Z-
dc.date.available2012-10-30T06:16:23Z-
dc.date.issued2001en_US
dc.identifier.citationPflugers Archiv European Journal Of Physiology, 2001, v. 442 n. 6, p. 903-909en_US
dc.identifier.issn0031-6768en_US
dc.identifier.urihttp://hdl.handle.net/10722/171689-
dc.description.abstractIn acute hypoxia, the release of nitric oxide (NO) produced in rat carotid body is unclear. The concentration of NO was measured electrochemically with a Pt/Nafion/Pd-IrOx/POAP-modified electrode placed on the surface of isolated carotid bodies superfused with bicarbonate-buffer saline at 35°C. In hypoxia, the concentration of NO in the carotid body was increased by 17±2 nM. The amount of NO release during hypoxia was augmented by increasing the number of carotid bodies surrounding the electrode and also in the presence of L-arginine. In addition, the hypoxia-induced elevation of NO was abolished by pretreatment with a nitric oxide synthase (NOS) inhibitor, L-NG-nitroarginine methylester (L-NAME). The results suggest that endogenous NO production in the carotid body increases during hypoxia. Electrophysiological measurement of single fiber activity in the sinus nerve revealed that L-NAME treatment enhances the afferent discharge in response to hypoxia. This confirms that the hypoxia-induced elevation of NO suppresses the carotid chemoreceptor response to hypoxia. Taken together, it is concluded that acute hypoxia increases NO generation in the rat carotid body, and that the elevated levels of NO suppress carotid chemoreceptor activity during hypoxia. Hence, NO may play an active inhibitory role in the control of carotid chemoreceptor activity during hypoxia.en_US
dc.languageengen_US
dc.publisherSpringer. The Journal's web site is located at http://link.springer.de/link/service/journals/00424/index.htmen_US
dc.relation.ispartofPflugers Archiv European Journal of Physiologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnoxia - Metabolismen_US
dc.subject.meshArginine - Pharmacologyen_US
dc.subject.meshCarotid Body - Metabolismen_US
dc.subject.meshChemoreceptor Cells - Drug Effects - Physiologyen_US
dc.subject.meshElectrodesen_US
dc.subject.meshEnzyme Inhibitors - Pharmacologyen_US
dc.subject.meshNg-Nitroarginine Methyl Ester - Pharmacologyen_US
dc.subject.meshNitric Oxide - Metabolismen_US
dc.subject.meshNitric Oxide Synthase - Antagonists & Inhibitorsen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.titleAcute hypoxia elevates nitric oxide generation in rat carotid body in vitroen_US
dc.typeArticleen_US
dc.identifier.emailFung, ML:fungml@hkucc.hku.hken_US
dc.identifier.authorityFung, ML=rp00433en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1007/s004240100610en_US
dc.identifier.pmid11680624-
dc.identifier.scopuseid_2-s2.0-0034808011en_US
dc.identifier.hkuros71887-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034808011&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume442en_US
dc.identifier.issue6en_US
dc.identifier.spage903en_US
dc.identifier.epage909en_US
dc.publisher.placeGermanyen_US
dc.identifier.scopusauthoridFung, ML=7101955092en_US
dc.identifier.scopusauthoridYe, JS=7403237793en_US
dc.identifier.scopusauthoridFung, PCW=7101613315en_US

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