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Article: Chronic hypoxia upregulates the expression and function of AT1 receptor in rat carotid body

TitleChronic hypoxia upregulates the expression and function of AT1 receptor in rat carotid body
Authors
Issue Date2000
PublisherSociety for Endocrinology. The Journal's web site is located at http://joe.endocrinology-journals.org
Citation
Journal Of Endocrinology, 2000, v. 167 n. 3, p. 517-524 How to Cite?
AbstractIn the present study, the effects of chronic hypoxia on the expression and localization of angiotensin II (Ang II) receptors are investigated by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and by immunohistochemistry. The effect of chronic hypoxia on the carotid body chemoreceptor activity was also examined by in vitro electrophysiology. Results from RT-PCR revealed that chronic hypoxia exhibited differential effects on the gene expression of Ang II receptors, namely AT1 and AT2, in the carotid body. The mRNA expression for subtypes of the AT1 receptor, AT1a and AT1b, was significantly increased in the carotid body with chronic hypoxia. To further investigate the localization of the AT1 receptor, an immunohistochemical study was performed. The results showed that AT1 receptor immunoreactivity was found in lobules of glomus cells in the carotid body and the immunoreactivity was more intense in chronic hypoxia than in normoxic controls. In vitro electrophysiological studies consistently demonstrated that chronic hypoxia enhanced the AT1 receptor-mediated excitation of carotid body chemoreceptor activity. These data suggest that chronic hypoxia upregulates the transcriptional and post-transcriptional expression of AT1 receptors in the rat carotid body. The upregulation of the expression also enhances AT1 receptor-mediated excitation of the carotid body afferent activity. This might be important in the modulation of cardiorespiratory functions as well as fluid and electrolyte homeostasis during chronic hypoxia.
Persistent Identifierhttp://hdl.handle.net/10722/171682
ISSN
2015 Impact Factor: 4.498
2015 SCImago Journal Rankings: 1.910
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLeung, PSen_US
dc.contributor.authorLam, SYen_US
dc.contributor.authorFung, MLen_US
dc.date.accessioned2012-10-30T06:16:20Z-
dc.date.available2012-10-30T06:16:20Z-
dc.date.issued2000en_US
dc.identifier.citationJournal Of Endocrinology, 2000, v. 167 n. 3, p. 517-524en_US
dc.identifier.issn0022-0795en_US
dc.identifier.urihttp://hdl.handle.net/10722/171682-
dc.description.abstractIn the present study, the effects of chronic hypoxia on the expression and localization of angiotensin II (Ang II) receptors are investigated by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and by immunohistochemistry. The effect of chronic hypoxia on the carotid body chemoreceptor activity was also examined by in vitro electrophysiology. Results from RT-PCR revealed that chronic hypoxia exhibited differential effects on the gene expression of Ang II receptors, namely AT1 and AT2, in the carotid body. The mRNA expression for subtypes of the AT1 receptor, AT1a and AT1b, was significantly increased in the carotid body with chronic hypoxia. To further investigate the localization of the AT1 receptor, an immunohistochemical study was performed. The results showed that AT1 receptor immunoreactivity was found in lobules of glomus cells in the carotid body and the immunoreactivity was more intense in chronic hypoxia than in normoxic controls. In vitro electrophysiological studies consistently demonstrated that chronic hypoxia enhanced the AT1 receptor-mediated excitation of carotid body chemoreceptor activity. These data suggest that chronic hypoxia upregulates the transcriptional and post-transcriptional expression of AT1 receptors in the rat carotid body. The upregulation of the expression also enhances AT1 receptor-mediated excitation of the carotid body afferent activity. This might be important in the modulation of cardiorespiratory functions as well as fluid and electrolyte homeostasis during chronic hypoxia.en_US
dc.languageengen_US
dc.publisherSociety for Endocrinology. The Journal's web site is located at http://joe.endocrinology-journals.orgen_US
dc.relation.ispartofJournal of Endocrinologyen_US
dc.subject.meshAngiotensin Ii - Pharmacologyen_US
dc.subject.meshAngiotensin Receptor Antagonistsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnoxia - Metabolismen_US
dc.subject.meshCarotid Body - Metabolismen_US
dc.subject.meshChemoreceptor Cells - Metabolismen_US
dc.subject.meshChronic Diseaseen_US
dc.subject.meshElectrophysiologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshGene Expression Regulationen_US
dc.subject.meshImmunohistochemistry - Methodsen_US
dc.subject.meshLosartan - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshRna, Messenger - Analysisen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshReceptor, Angiotensin, Type 1en_US
dc.subject.meshReceptor, Angiotensin, Type 2en_US
dc.subject.meshReceptors, Angiotensin - Analysis - Geneticsen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.titleChronic hypoxia upregulates the expression and function of AT1 receptor in rat carotid bodyen_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.doi10.1677/joe.0.1670517en_US
dc.identifier.pmid11115779-
dc.identifier.scopuseid_2-s2.0-0034519341en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034519341&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume167en_US
dc.identifier.issue3en_US
dc.identifier.spage517en_US
dc.identifier.epage524en_US
dc.identifier.isiWOS:000167209500018-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridLeung, PS=7401748938en_US
dc.identifier.scopusauthoridLam, SY=7402279518en_US
dc.identifier.scopusauthoridFung, ML=7101955092en_US

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