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Article: Renin-angiotensin system in the carotid body

TitleRenin-angiotensin system in the carotid body
Authors
KeywordsAT1 receptor
Carotid body
Hypoxia
Renin-angiotensin system
Issue Date2003
PublisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/biocel
Citation
International Journal Of Biochemistry And Cell Biology, 2003, v. 35 n. 6, p. 847-854 How to Cite?
AbstractResearch studies have been done on the influence of the renin-angiotensin system (RAS) on numerous tissues and organs. The local RAS, which is frequently of paracrine/autocrine origin, caters to specific organ and tissue needs through actions that add to, or differ from, the circulating RAS. Recent data have demonstrated a functional expression of RAS in the carotid body, wherein the carotid chemoreceptors play a major physiological role in the regulation of autonomic responses to changes in arterial chemical content. However, the angiotensin II and other vasoactive substances can directly modulate the excitability of the chemoreceptor. Long-term hypoxia modifies the level of gene expression in the carotid body by increasing the expression of AT1 receptors along with sensitivity of the chemoreceptor to angiotensin II. Even though these findings support a physiological role of RAS in the carotid body, it has yet to be clearly defined. As a result this review will present current information about expression and localization of AT1 receptors, and show that local RAS exists in the carotid body. The regulation of RAS by chronic hypoxia, the significance of its changes and clinical relevance in the carotid body, are also addressed. © 2003 Elsevier Science Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/81127
ISSN
2015 Impact Factor: 3.905
2015 SCImago Journal Rankings: 2.003
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLeung, PSen_HK
dc.contributor.authorFung, MLen_HK
dc.contributor.authorTam, MSCen_HK
dc.date.accessioned2010-09-06T08:14:08Z-
dc.date.available2010-09-06T08:14:08Z-
dc.date.issued2003en_HK
dc.identifier.citationInternational Journal Of Biochemistry And Cell Biology, 2003, v. 35 n. 6, p. 847-854en_HK
dc.identifier.issn1357-2725en_HK
dc.identifier.urihttp://hdl.handle.net/10722/81127-
dc.description.abstractResearch studies have been done on the influence of the renin-angiotensin system (RAS) on numerous tissues and organs. The local RAS, which is frequently of paracrine/autocrine origin, caters to specific organ and tissue needs through actions that add to, or differ from, the circulating RAS. Recent data have demonstrated a functional expression of RAS in the carotid body, wherein the carotid chemoreceptors play a major physiological role in the regulation of autonomic responses to changes in arterial chemical content. However, the angiotensin II and other vasoactive substances can directly modulate the excitability of the chemoreceptor. Long-term hypoxia modifies the level of gene expression in the carotid body by increasing the expression of AT1 receptors along with sensitivity of the chemoreceptor to angiotensin II. Even though these findings support a physiological role of RAS in the carotid body, it has yet to be clearly defined. As a result this review will present current information about expression and localization of AT1 receptors, and show that local RAS exists in the carotid body. The regulation of RAS by chronic hypoxia, the significance of its changes and clinical relevance in the carotid body, are also addressed. © 2003 Elsevier Science Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/biocelen_HK
dc.relation.ispartofInternational Journal of Biochemistry and Cell Biologyen_HK
dc.subjectAT1 receptoren_HK
dc.subjectCarotid bodyen_HK
dc.subjectHypoxiaen_HK
dc.subjectRenin-angiotensin systemen_HK
dc.titleRenin-angiotensin system in the carotid bodyen_HK
dc.typeArticleen_HK
dc.identifier.emailFung, ML: fungml@hkucc.hku.hken_HK
dc.identifier.authorityFung, ML=rp00433en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S1357-2725(02)00180-2en_HK
dc.identifier.pmid12676171en_HK
dc.identifier.scopuseid_2-s2.0-0037409223en_HK
dc.identifier.hkuros83576en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037409223&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume35en_HK
dc.identifier.issue6en_HK
dc.identifier.spage847en_HK
dc.identifier.epage854en_HK
dc.identifier.isiWOS:000182501200013-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLeung, PS=7401748938en_HK
dc.identifier.scopusauthoridFung, ML=7101955092en_HK
dc.identifier.scopusauthoridTam, MSC=36873540800en_HK

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