File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Chronic hypoxia enhances endothelin-1-induced intracellular calcium elevation in rat carotid body chemoreceptors and up-regulates ETA receptor expression

TitleChronic hypoxia enhances endothelin-1-induced intracellular calcium elevation in rat carotid body chemoreceptors and up-regulates ETA receptor expression
Authors
KeywordsCarotid body
Endothelin
Endothelin receptor
ET-1
ETA receptors
Glomus cell
Respiration
Type-I cell
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. 443 n. 4, p. 565-573 How to Cite?
AbstractEndothelin-1 (ET-1) excites carotid body (CB) chemoreceptors and induces mitosis of the chemoreceptors in chronic hypoxia. The aim of the present study was to examine the hypothesis that up-regulation of both ETA receptor and endogenous ET-1 expression in CB chemoreceptors enhances the response of intracellular Ca2+ to ET-1 following adaptation to chronic hypoxia (10% inspired O2 for 3-4 weeks). Cytosolic free [Ca2+] ([Ca2+]i) in type-I (glomus) cells freshly dissociated from rat CBs was measured by spectrofluorometry. Application of exogenous ET-1 (1-100 nM) pendently elevated [Ca2+]i in the glomus cells. The response to ET-1 (100 nM) was 49% greater in the chronically hypoxic (CH) group. The ET-1 response was abolished completely by the ETA receptor antagonist BQ610 (1 μM), but not by the ETB antagonist BQ788 (1 μM). The transient [Ca2+]i elevation induced by caffeine (30 mM) in the normoxic group was similar to that in the CH group, suggesting no differences in the intracellular Ca2+ stores. In situ hybridization with a digoxigenin-labelled antisense ETA receptor mRNA oligonucleotide probe revealed very intense and ubiquitous specific expression of ETA receptors in the lobules of glomus cells in the CH group, whereas staining in normoxic controls was light. Immunohistochemical studies revealed intense cytoplasmic staining for ET-1-immunoreactivity in most of the cell clusters in glomera in the CBs of CH rats but was faint in normoxic CBs. These findings indicate increased expression of both the ETA receptor and ET-1 in CB chemoreceptors during chronic hypoxia. Taken together, our results suggest that the [Ca2+]i response to ET-1 in rat CB chemoreceptors is augmented by up-regulation of ETA receptors and ET-1 expression. The enhancement of the paracrine/autocrine effect of ET-1 on the chemoreceptors is consistent with an excitatory and mitogenic role of the ET-1 and ETA receptor in the CB during chronic hypoxia.
Persistent Identifierhttp://hdl.handle.net/10722/149606
ISSN
2015 Impact Factor: 3.654
2015 SCImago Journal Rankings: 1.638
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChen, Yen_HK
dc.contributor.authorTipoe, GLen_HK
dc.contributor.authorLiong, Een_HK
dc.contributor.authorLeung, Pen_HK
dc.contributor.authorLam, SYen_HK
dc.contributor.authorIwase, Ren_HK
dc.contributor.authorTjong, YWen_HK
dc.contributor.authorFung, MLen_HK
dc.date.accessioned2012-06-26T05:55:52Z-
dc.date.available2012-06-26T05:55:52Z-
dc.date.issued2002en_HK
dc.identifier.citationPflugers Archiv European Journal Of Physiology, 2002, v. 443 n. 4, p. 565-573en_HK
dc.identifier.issn0031-6768en_HK
dc.identifier.urihttp://hdl.handle.net/10722/149606-
dc.description.abstractEndothelin-1 (ET-1) excites carotid body (CB) chemoreceptors and induces mitosis of the chemoreceptors in chronic hypoxia. The aim of the present study was to examine the hypothesis that up-regulation of both ETA receptor and endogenous ET-1 expression in CB chemoreceptors enhances the response of intracellular Ca2+ to ET-1 following adaptation to chronic hypoxia (10% inspired O2 for 3-4 weeks). Cytosolic free [Ca2+] ([Ca2+]i) in type-I (glomus) cells freshly dissociated from rat CBs was measured by spectrofluorometry. Application of exogenous ET-1 (1-100 nM) pendently elevated [Ca2+]i in the glomus cells. The response to ET-1 (100 nM) was 49% greater in the chronically hypoxic (CH) group. The ET-1 response was abolished completely by the ETA receptor antagonist BQ610 (1 μM), but not by the ETB antagonist BQ788 (1 μM). The transient [Ca2+]i elevation induced by caffeine (30 mM) in the normoxic group was similar to that in the CH group, suggesting no differences in the intracellular Ca2+ stores. In situ hybridization with a digoxigenin-labelled antisense ETA receptor mRNA oligonucleotide probe revealed very intense and ubiquitous specific expression of ETA receptors in the lobules of glomus cells in the CH group, whereas staining in normoxic controls was light. Immunohistochemical studies revealed intense cytoplasmic staining for ET-1-immunoreactivity in most of the cell clusters in glomera in the CBs of CH rats but was faint in normoxic CBs. These findings indicate increased expression of both the ETA receptor and ET-1 in CB chemoreceptors during chronic hypoxia. Taken together, our results suggest that the [Ca2+]i response to ET-1 in rat CB chemoreceptors is augmented by up-regulation of ETA receptors and ET-1 expression. The enhancement of the paracrine/autocrine effect of ET-1 on the chemoreceptors is consistent with an excitatory and mitogenic role of the ET-1 and ETA receptor in the CB during chronic hypoxia.en_HK
dc.languageengen_US
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.subjectEndothelinen_HK
dc.subjectEndothelin receptoren_HK
dc.subjectET-1en_HK
dc.subjectETA receptorsen_HK
dc.subjectGlomus cellen_HK
dc.subjectRespirationen_HK
dc.subjectType-I cellen_HK
dc.subject.meshAdaptation, Physiological - Physiologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnoxia - Metabolismen_US
dc.subject.meshCalcium - Metabolismen_US
dc.subject.meshCarotid Body - Metabolismen_US
dc.subject.meshChemoreceptor Cells - Metabolismen_US
dc.subject.meshChronic Diseaseen_US
dc.subject.meshEndothelin-1 - Metabolism - Pharmacologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshIn Situ Hybridizationen_US
dc.subject.meshMaleen_US
dc.subject.meshMitosis - Physiologyen_US
dc.subject.meshRna, Messenger - Analysisen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshReceptor, Endothelin Aen_US
dc.subject.meshReceptors, Endothelin - Genetics - Metabolismen_US
dc.subject.meshUp-Regulation - Physiologyen_US
dc.titleChronic hypoxia enhances endothelin-1-induced intracellular calcium elevation in rat carotid body chemoreceptors and up-regulates ETA receptor expressionen_HK
dc.typeArticleen_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_fulltexten_US
dc.identifier.doi10.1007/s00424-001-0728-2en_HK
dc.identifier.pmid11907823-
dc.identifier.scopuseid_2-s2.0-0036185347en_HK
dc.identifier.hkuros71890-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036185347&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume443en_HK
dc.identifier.issue4en_HK
dc.identifier.spage565en_HK
dc.identifier.epage573en_HK
dc.identifier.isiWOS:000174363000008-
dc.publisher.placeGermanyen_HK
dc.identifier.scopusauthoridChen, Y=7601439932en_HK
dc.identifier.scopusauthoridTipoe, GL=7003550610en_HK
dc.identifier.scopusauthoridLiong, E=6602732210en_HK
dc.identifier.scopusauthoridLeung, P=7401748938en_HK
dc.identifier.scopusauthoridLam, SY=7402279518en_HK
dc.identifier.scopusauthoridIwase, R=15823491500en_HK
dc.identifier.scopusauthoridTjong, YW=6507176524en_HK
dc.identifier.scopusauthoridFung, ML=7101955092en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats