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Article: Attenuated "cross talk" between κ-opioid receptors and β-adrenoceptors in the heart of chronically hypoxic rats

TitleAttenuated "cross talk" between κ-opioid receptors and β-adrenoceptors in the heart of chronically hypoxic rats
Authors
Shan, JYu, XCFung, MLWong, TM
Keywordsβ-Adrenoceptor
κ-Opioid receptor
Adenylyl cyclase
cAMP
Chronic hypoxia
Gs-protein
Heart
Intracellular Ca2+ transient
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. 444 n. 1-2, p. 126-132 How to Cite?
DOI: http://dx.doi.org/10.1007/s00424-002-0814-0
AbstractAt 0.1-1 μM, U50488H, a κ-opioid receptor agonist, inhibited the stimulatory effects of 1 μM isoprenaline, a β-adrenoceptor agonist, on the electrically induced intracellular Ca2+ ([Ca2+]i) transient and cAMP accumulation ("cross talk" between κ-opioid receptors and β-adrenoceptors) in the presence of 1 μM ICI118,551, a β2-adrenoceptor antagonist in ventricular myocytes from both normoxic and chronically hypoxic rats. Pretreatment with 20 μg/ml cholera toxin increased the ADP-ribosylation of Gsα subunits and the electrically induced [Ca2+]i transient in both normoxic and chronically hypoxic rats. The effects of cholera toxin were inhibited by 1 μM U50488H and the inhibitory effect of U50488H was attenuated in chronically hypoxic rats. Similarly, 1 μM forskolin also increased the electrically induced [Ca2+]i transient and cAMP accumulation, which were both inhibited by U50488H, in both normoxic and chronically hypoxic rats. The inhibitory effects of 1 μM U50488H were significantly attenuated in chronically hypoxic rats. The results are novel findings, in that the "cross talk" between κ-opioid receptors and β-adrenoceptors is attenuated following chronic hypoxia. The attenuation may be due to decreased responses of Gs-protein and adenylyl cyclase to κ-opioid receptor activation in addition to desensitization of the receptor itself.
Persistent Identifierhttp://hdl.handle.net/10722/171705
ISSN
0031-6768
2023 Impact Factor: 2.9
2023 SCImago Journal Rankings: 1.361
ISI Accession Number ID
WOS:000175781400013
References
References in Scopus

 

DC FieldValueLanguage
dc.contributor.authorShan, Jen_US
dc.contributor.authorYu, XCen_US
dc.contributor.authorFung, MLen_US
dc.contributor.authorWong, TMen_US
dc.date.accessioned2012-10-30T06:16:30Z-
dc.date.available2012-10-30T06:16:30Z-
dc.date.issued2002en_US
dc.identifier.citationPflugers Archiv European Journal Of Physiology, 2002, v. 444 n. 1-2, p. 126-132en_US
dc.identifier.issn0031-6768en_US
dc.identifier.urihttp://hdl.handle.net/10722/171705-
dc.description.abstractAt 0.1-1 μM, U50488H, a κ-opioid receptor agonist, inhibited the stimulatory effects of 1 μM isoprenaline, a β-adrenoceptor agonist, on the electrically induced intracellular Ca2+ ([Ca2+]i) transient and cAMP accumulation ("cross talk" between κ-opioid receptors and β-adrenoceptors) in the presence of 1 μM ICI118,551, a β2-adrenoceptor antagonist in ventricular myocytes from both normoxic and chronically hypoxic rats. Pretreatment with 20 μg/ml cholera toxin increased the ADP-ribosylation of Gsα subunits and the electrically induced [Ca2+]i transient in both normoxic and chronically hypoxic rats. The effects of cholera toxin were inhibited by 1 μM U50488H and the inhibitory effect of U50488H was attenuated in chronically hypoxic rats. Similarly, 1 μM forskolin also increased the electrically induced [Ca2+]i transient and cAMP accumulation, which were both inhibited by U50488H, in both normoxic and chronically hypoxic rats. The inhibitory effects of 1 μM U50488H were significantly attenuated in chronically hypoxic rats. The results are novel findings, in that the "cross talk" between κ-opioid receptors and β-adrenoceptors is attenuated following chronic hypoxia. The attenuation may be due to decreased responses of Gs-protein and adenylyl cyclase to κ-opioid receptor activation in addition to desensitization of the receptor itself.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.subjectβ-Adrenoceptor-
dc.subjectκ-Opioid receptor-
dc.subjectAdenylyl cyclase-
dc.subjectcAMP-
dc.subjectChronic hypoxia-
dc.subjectGs-protein-
dc.subjectHeart-
dc.subjectIntracellular Ca2+ transient-
dc.subject.meshAdenosine Diphosphate Ribose - Metabolismen_US
dc.subject.meshAdenylate Cyclase - Metabolismen_US
dc.subject.meshAdrenergic Beta-Agonists - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnoxia - Physiopathologyen_US
dc.subject.meshCalcium Signaling - Drug Effectsen_US
dc.subject.meshCardiomegaly - Physiopathologyen_US
dc.subject.meshCholera Toxin - Pharmacologyen_US
dc.subject.meshChronic Diseaseen_US
dc.subject.meshCyclic Amp - Metabolismen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshFluorescent Dyesen_US
dc.subject.meshForskolin - Pharmacologyen_US
dc.subject.meshFura-2en_US
dc.subject.meshGtp-Binding Protein Alpha Subunits, Gs - Metabolismen_US
dc.subject.meshHeart - Physiopathologyen_US
dc.subject.meshIsoproterenol - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshReceptor Cross-Talk - Physiologyen_US
dc.subject.meshReceptors, Adrenergic, Beta - Physiologyen_US
dc.subject.meshReceptors, Opioid, Kappa - Physiologyen_US
dc.titleAttenuated "cross talk" between κ-opioid receptors and β-adrenoceptors in the heart of chronically hypoxic ratsen_US
dc.typeArticleen_US
dc.identifier.emailFung, ML:fungml@hkucc.hku.hken_US
dc.identifier.emailWong, TM: tm.wong@hkuspace.hku.hk-
dc.identifier.authorityFung, ML=rp00433en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1007/s00424-002-0814-0en_US
dc.identifier.pmid11976924-
dc.identifier.scopuseid_2-s2.0-0036261285en_US
dc.identifier.hkuros71971-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036261285&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume444en_US
dc.identifier.issue1-2en_US
dc.identifier.spage126en_US
dc.identifier.epage132en_US
dc.identifier.isiWOS:000175781400013-
dc.publisher.placeGermanyen_US
dc.identifier.scopusauthoridShan, J=9272965300en_US
dc.identifier.scopusauthoridYu, XC=7404114600en_US
dc.identifier.scopusauthoridFung, ML=7101955092en_US
dc.identifier.scopusauthoridWong, TM=7403531434en_US
dc.identifier.issnl0031-6768-

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