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Article: Impaired G(s)α and adenylyl cyclase cause β-adrenoceptor desensitization in chronically hypoxic rat hearts
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TitleImpaired G(s)α and adenylyl cyclase cause β-adrenoceptor desensitization in chronically hypoxic rat hearts
 
AuthorsPei, JM1
Yu, XC1
Fung, ML1 1
Zhou, JJ1
Cheung, CS1
Wong, NS1
Leung, MP1 1
Wong, TM1 1 1
 
KeywordsCardiac hypertrophy
G protein
 
Issue Date2000
 
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpcell.physiology.org/
 
CitationAmerican 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.
 
ISSN0363-6143
2012 Impact Factor: 3.711
2012 SCImago Journal Rankings: 1.643
 
ISI Accession Number IDWOS:000089790300018
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorPei, JM
 
dc.contributor.authorYu, XC
 
dc.contributor.authorFung, ML
 
dc.contributor.authorZhou, JJ
 
dc.contributor.authorCheung, CS
 
dc.contributor.authorWong, NS
 
dc.contributor.authorLeung, MP
 
dc.contributor.authorWong, TM
 
dc.date.accessioned2012-05-29T06:03:46Z
 
dc.date.available2012-05-29T06:03:46Z
 
dc.date.issued2000
 
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.
 
dc.description.naturelink_to_OA_fulltext
 
dc.identifier.citationAmerican Journal of Physiology - Cell Physiology, 2000, v. 279 n. 5 48-5, p. C1455-C1463 [How to Cite?]
 
dc.identifier.epageC1463
 
dc.identifier.hkuros61139
 
dc.identifier.isiWOS:000089790300018
 
dc.identifier.issn0363-6143
2012 Impact Factor: 3.711
2012 SCImago Journal Rankings: 1.643
 
dc.identifier.issue5 48-5
 
dc.identifier.pmid11029293
 
dc.identifier.scopuseid_2-s2.0-0033697030
 
dc.identifier.spageC1455
 
dc.identifier.urihttp://hdl.handle.net/10722/147445
 
dc.identifier.volume279
 
dc.languageeng
 
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpcell.physiology.org/
 
dc.publisher.placeUnited States
 
dc.relation.ispartofAmerican Journal of Physiology - Cell Physiology
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshAdenylate Cyclase - Physiology
 
dc.subject.meshAnimals
 
dc.subject.meshAnoxia - Physiopathology
 
dc.subject.meshCalcium - Metabolism
 
dc.subject.meshCardiotonic Agents - Pharmacology
 
dc.subject.meshCholera Toxin - Pharmacology
 
dc.subject.meshChronic Disease
 
dc.subject.meshCyclic Amp - Metabolism
 
dc.subject.meshElectric Stimulation
 
dc.subject.meshForskolin - Pharmacology
 
dc.subject.meshGtp-Binding Protein Alpha Subunits, Gs - Physiology
 
dc.subject.meshHeart Ventricles
 
dc.subject.meshIntracellular Membranes - Metabolism
 
dc.subject.meshIsoproterenol - Pharmacology
 
dc.subject.meshMale
 
dc.subject.meshMyocardium - Metabolism - Pathology
 
dc.subject.meshProtein Isoforms - Physiology
 
dc.subject.meshRats
 
dc.subject.meshRats, Sprague-Dawley
 
dc.subject.meshReceptors, Adrenergic, Beta - Metabolism
 
dc.subject.meshReference Values
 
dc.subject.meshSodium Fluoride - Pharmacology
 
dc.subjectCardiac hypertrophy
 
dc.subjectG protein
 
dc.titleImpaired G(s)α and adenylyl cyclase cause β-adrenoceptor desensitization in chronically hypoxic rat hearts
 
dc.typeArticle
 
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Author Affiliations
  1. The University of Hong Kong