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Article: Chronic hypoxia modulates the function and expression of melatonin receptors in the rat carotid body

TitleChronic hypoxia modulates the function and expression of melatonin receptors in the rat carotid body
Authors
KeywordsCarotid chemoreceptor
Chronic hypoxia
Circadian
Melatonin
Melatonin receptors
Type-I cells
Issue Date2006
PublisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/JPI
Citation
Journal Of Pineal Research, 2006, v. 40 n. 2, p. 125-134 How to Cite?
AbstractMelatonin modulates the carotid chemoreceptor response to chemical stimuli, and chronic hypoxia changes circadian activities and carotid body function. The purpose of this study was to test the hypothesis that chronic hypoxia alters the function and expression of melatonin receptors in the rat carotid body. Effects of melatonin on the carotid responses to hypercapnic acidosis and to hypoxia were determined by spectrofluorometric measurement of cytosolic calcium ([Ca2+]i) in fura-2-loaded type-I (glomus) cells dissociated from carotid bodies obtained from normoxic (Nx) or chronically hypoxic (CH) rats breathing 10% oxygen for 4 wk. In the Nx control, melatonin concentration dependently attenuated the peak [Ca2+]i response to hypercapnic acidosis, whereas it augmented the [Ca 2+]i response to cyanide or deoxygenated buffer. Yet, melatonin enhanced the peak [Ca2+]i responses to hypercapnic acidosis or hypoxia in the CH glomus cells. An agonist of melatonin receptors, iodomelatonin also elevated the hypercapnic or hypoxic responses in the CH groups. The melatonin-induced changes in the [Ca2+] i responses were abolished by pretreatment with nonselective mt 1/MT2 antagonist, luzindole, and by MT2 antagonists, 4-phenyl-2-propionamidotetraline or DH97. These findings suggest a functional modulation of melatonin receptors in the glomus cells in chronic hypoxia. To evaluate the level of expression of the melatonin receptors, in situ hybridization study with antisense mt1 and MT2 receptor mRNA oligonucleotide probes was performed on the Nx and CH carotid bodies. There were significant increases in the expression of mt1 and MT 2 receptors in the CH comparing with the Nx group. Taken together, our results suggest an upregulation of the carotid expression of melatonin receptors by chronic hypoxia, which modulates the carotid response to melatonin for the circadian influence on breathing. © 2005 Blackwell Munksgaard.
Persistent Identifierhttp://hdl.handle.net/10722/67834
ISSN
2015 Impact Factor: 9.314
2015 SCImago Journal Rankings: 2.655
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTjong, YWen_HK
dc.contributor.authorChen, Yen_HK
dc.contributor.authorLiong, ECen_HK
dc.contributor.authorTipoe, GLen_HK
dc.contributor.authorFung, MLen_HK
dc.date.accessioned2010-09-06T05:58:41Z-
dc.date.available2010-09-06T05:58:41Z-
dc.date.issued2006en_HK
dc.identifier.citationJournal Of Pineal Research, 2006, v. 40 n. 2, p. 125-134en_HK
dc.identifier.issn0742-3098en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67834-
dc.description.abstractMelatonin modulates the carotid chemoreceptor response to chemical stimuli, and chronic hypoxia changes circadian activities and carotid body function. The purpose of this study was to test the hypothesis that chronic hypoxia alters the function and expression of melatonin receptors in the rat carotid body. Effects of melatonin on the carotid responses to hypercapnic acidosis and to hypoxia were determined by spectrofluorometric measurement of cytosolic calcium ([Ca2+]i) in fura-2-loaded type-I (glomus) cells dissociated from carotid bodies obtained from normoxic (Nx) or chronically hypoxic (CH) rats breathing 10% oxygen for 4 wk. In the Nx control, melatonin concentration dependently attenuated the peak [Ca2+]i response to hypercapnic acidosis, whereas it augmented the [Ca 2+]i response to cyanide or deoxygenated buffer. Yet, melatonin enhanced the peak [Ca2+]i responses to hypercapnic acidosis or hypoxia in the CH glomus cells. An agonist of melatonin receptors, iodomelatonin also elevated the hypercapnic or hypoxic responses in the CH groups. The melatonin-induced changes in the [Ca2+] i responses were abolished by pretreatment with nonselective mt 1/MT2 antagonist, luzindole, and by MT2 antagonists, 4-phenyl-2-propionamidotetraline or DH97. These findings suggest a functional modulation of melatonin receptors in the glomus cells in chronic hypoxia. To evaluate the level of expression of the melatonin receptors, in situ hybridization study with antisense mt1 and MT2 receptor mRNA oligonucleotide probes was performed on the Nx and CH carotid bodies. There were significant increases in the expression of mt1 and MT 2 receptors in the CH comparing with the Nx group. Taken together, our results suggest an upregulation of the carotid expression of melatonin receptors by chronic hypoxia, which modulates the carotid response to melatonin for the circadian influence on breathing. © 2005 Blackwell Munksgaard.en_HK
dc.languageengen_HK
dc.publisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/JPIen_HK
dc.relation.ispartofJournal of Pineal Researchen_HK
dc.subjectCarotid chemoreceptoren_HK
dc.subjectChronic hypoxiaen_HK
dc.subjectCircadianen_HK
dc.subjectMelatoninen_HK
dc.subjectMelatonin receptorsen_HK
dc.subjectType-I cellsen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAnoxia - metabolism - pathologyen_HK
dc.subject.meshCalcium - metabolismen_HK
dc.subject.meshCarotid Body - metabolism - pathologyen_HK
dc.subject.meshChronic Diseaseen_HK
dc.subject.meshHypercapnia - metabolismen_HK
dc.subject.meshRatsen_HK
dc.subject.meshReceptors, Melatonin - antagonists & inhibitors - metabolismen_HK
dc.subject.meshUp-Regulationen_HK
dc.titleChronic hypoxia modulates the function and expression of melatonin receptors in the rat carotid bodyen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0742-3098&volume=40&issue=2&spage=125&epage=134&date=2006&atitle=Chronic+hypoxia+modulates+the+function+and+expression+of+melatonin+receptors+in+the+rat+carotid+bodyen_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.doi10.1111/j.1600-079X.2005.00286.xen_HK
dc.identifier.pmid16441549-
dc.identifier.scopuseid_2-s2.0-33645109253en_HK
dc.identifier.hkuros122289en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33645109253&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume40en_HK
dc.identifier.issue2en_HK
dc.identifier.spage125en_HK
dc.identifier.epage134en_HK
dc.identifier.isiWOS:000234985200004-
dc.publisher.placeDenmarken_HK
dc.identifier.scopusauthoridTjong, YW=6507176524en_HK
dc.identifier.scopusauthoridChen, Y=7601439932en_HK
dc.identifier.scopusauthoridLiong, EC=6602732210en_HK
dc.identifier.scopusauthoridTipoe, GL=7003550610en_HK
dc.identifier.scopusauthoridFung, ML=7101955092en_HK
dc.identifier.citeulike487223-

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