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Article: Impaired G(s)α and adenylyl cyclase cause β-adrenoceptor desensitization in chronically hypoxic rat hearts

TitleImpaired G(s)α and adenylyl cyclase cause β-adrenoceptor desensitization in chronically hypoxic rat hearts
Authors
KeywordsCardiac hypertrophy
G protein
Issue Date2000
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpcell.physiology.org/
Citation
American Journal of Physiology - Cell Physiology, 2000, v. 279 n. 5 48-5, p. C1455-C1463 How to Cite?
AbstractThe effects of β-adrenoceptor stimulation with isoproterenol on electrically induced contraction and intracellular calcium ([Ca2+](i)) transient, and cAMP in myocytes from both hypertrophied right and non-hypertrophied left ventricles of rats exposed to 10% oxygen for 4 wk, were significantly attenuated. The increased [Ca2+](i) transient in response to cholera toxin was abolished, whereas increased cAMP after NaF significantly attenuated. The biologically active isoform, G(s)α-small (45 kDa), was reduced while the biologically inactive isoform, G(s)α-large (52 kDa), increased. The increased electrically induced [Ca2+](i) transient and cAMP with 10-100 μM forskolin were significantly attenuated in chronically hypoxic rats. The content of G(i)α2, the predominant isoform of G(i) protein in the heart, was unchanged. Results indicate that impaired functions of G(s) protein and adenylyl cyclase cause β-adrenoceptor desensitization. The impaired function of the G(s) protein may be due to reduced G(s)α-small and/or increased G(s)α-large, which does not result from changes in G(i) protein. Responses to all treatments were the same for right and left ventricles, indicating that the impaired cardiac functions are not secondary to cardiac hypertrophy.
Persistent Identifierhttp://hdl.handle.net/10722/147445
ISSN
2014 Impact Factor: 3.780
2014 SCImago Journal Rankings: 1.667
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorPei, JMen_HK
dc.contributor.authorYu, XCen_HK
dc.contributor.authorFung, MLen_HK
dc.contributor.authorZhou, JJen_HK
dc.contributor.authorCheung, CSen_HK
dc.contributor.authorWong, NSen_HK
dc.contributor.authorLeung, MPen_HK
dc.contributor.authorWong, TMen_HK
dc.date.accessioned2012-05-29T06:03:46Z-
dc.date.available2012-05-29T06:03:46Z-
dc.date.issued2000en_HK
dc.identifier.citationAmerican Journal of Physiology - Cell Physiology, 2000, v. 279 n. 5 48-5, p. C1455-C1463en_HK
dc.identifier.issn0363-6143en_HK
dc.identifier.urihttp://hdl.handle.net/10722/147445-
dc.description.abstractThe effects of β-adrenoceptor stimulation with isoproterenol on electrically induced contraction and intracellular calcium ([Ca2+](i)) transient, and cAMP in myocytes from both hypertrophied right and non-hypertrophied left ventricles of rats exposed to 10% oxygen for 4 wk, were significantly attenuated. The increased [Ca2+](i) transient in response to cholera toxin was abolished, whereas increased cAMP after NaF significantly attenuated. The biologically active isoform, G(s)α-small (45 kDa), was reduced while the biologically inactive isoform, G(s)α-large (52 kDa), increased. The increased electrically induced [Ca2+](i) transient and cAMP with 10-100 μM forskolin were significantly attenuated in chronically hypoxic rats. The content of G(i)α2, the predominant isoform of G(i) protein in the heart, was unchanged. Results indicate that impaired functions of G(s) protein and adenylyl cyclase cause β-adrenoceptor desensitization. The impaired function of the G(s) protein may be due to reduced G(s)α-small and/or increased G(s)α-large, which does not result from changes in G(i) protein. Responses to all treatments were the same for right and left ventricles, indicating that the impaired cardiac functions are not secondary to cardiac hypertrophy.en_HK
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpcell.physiology.org/en_HK
dc.relation.ispartofAmerican Journal of Physiology - Cell Physiologyen_HK
dc.subjectCardiac hypertrophyen_HK
dc.subjectG proteinen_HK
dc.subject.meshAdenylate Cyclase - Physiologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnoxia - Physiopathologyen_US
dc.subject.meshCalcium - Metabolismen_US
dc.subject.meshCardiotonic Agents - Pharmacologyen_US
dc.subject.meshCholera Toxin - Pharmacologyen_US
dc.subject.meshChronic Diseaseen_US
dc.subject.meshCyclic Amp - Metabolismen_US
dc.subject.meshElectric Stimulationen_US
dc.subject.meshForskolin - Pharmacologyen_US
dc.subject.meshGtp-Binding Protein Alpha Subunits, Gs - Physiologyen_US
dc.subject.meshHeart Ventriclesen_US
dc.subject.meshIntracellular Membranes - Metabolismen_US
dc.subject.meshIsoproterenol - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMyocardium - Metabolism - Pathologyen_US
dc.subject.meshProtein Isoforms - Physiologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshReceptors, Adrenergic, Beta - Metabolismen_US
dc.subject.meshReference Valuesen_US
dc.subject.meshSodium Fluoride - Pharmacologyen_US
dc.titleImpaired G(s)α and adenylyl cyclase cause β-adrenoceptor desensitization in chronically hypoxic rat heartsen_HK
dc.typeArticleen_HK
dc.identifier.emailFung, ML: fungml@hkucc.hku.hken_HK
dc.identifier.emailWong, NS: nswong@hkucc.hku.hken_HK
dc.identifier.emailLeung, MP: mpleung@hkucc.hku.hken_HK
dc.identifier.authorityFung, ML=rp00433en_HK
dc.identifier.authorityWong, NS=rp00340en_HK
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.pmid11029293en_HK
dc.identifier.scopuseid_2-s2.0-0033697030en_HK
dc.identifier.hkuros61139-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033697030&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume279en_HK
dc.identifier.issue5 48-5en_HK
dc.identifier.spageC1455en_HK
dc.identifier.epageC1463en_HK
dc.identifier.isiWOS:000089790300018-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridPei, JM=7103299061en_HK
dc.identifier.scopusauthoridYu, XC=7404114600en_HK
dc.identifier.scopusauthoridFung, ML=7101955092en_HK
dc.identifier.scopusauthoridZhou, JJ=7405545441en_HK
dc.identifier.scopusauthoridCheung, CS=7202061710en_HK
dc.identifier.scopusauthoridWong, NS=7202836641en_HK
dc.identifier.scopusauthoridLeung, MP=7201944800en_HK
dc.identifier.scopusauthoridWong, TM=7403531434en_HK

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