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

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Title	Impaired G(s)α and adenylyl cyclase cause β-adrenoceptor desensitization in chronically hypoxic rat hearts
Authors	Pei, JM1 Yu, XC1 Fung, ML1 Zhou, JJ1 Cheung, CS1 Wong, NS1 Leung, MP1 Wong, TM1
Keywords	Cardiac hypertrophy G protein
Issue Date	2000
Publisher	American 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?]
Abstract	The 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.
ISSN	0363-6143 2011 Impact Factor: 3.536 2011 SCImago Journal Rankings: 0.447
ISI Accession Number ID	WOS:000089790300018
References	References in Scopus

DC Field	Value
dc.contributor.author	Pei, JM
dc.contributor.author	Yu, XC
dc.contributor.author	Fung, ML
dc.contributor.author	Zhou, JJ
dc.contributor.author	Cheung, CS
dc.contributor.author	Wong, NS
dc.contributor.author	Leung, MP
dc.contributor.author	Wong, TM
dc.date.accessioned	2012-05-29T06:03:46Z
dc.date.available	2012-05-29T06:03:46Z
dc.date.issued	2000
dc.description.abstract	The 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.nature	link_to_OA_fulltext
dc.identifier.citation	American Journal of Physiology - Cell Physiology, 2000, v. 279 n. 5 48-5, p. C1455-C1463 [How to Cite?]
dc.identifier.epage	C1463
dc.identifier.hkuros	61139
dc.identifier.isi	WOS:000089790300018
dc.identifier.issn	0363-6143 2011 Impact Factor: 3.536 2011 SCImago Journal Rankings: 0.447
dc.identifier.issue	5 48-5
dc.identifier.pmid	11029293
dc.identifier.scopus	eid_2-s2.0-0033697030
dc.identifier.spage	C1455
dc.identifier.uri	http://hdl.handle.net/10722/147445
dc.identifier.volume	279
dc.language	eng
dc.publisher	American Physiological Society. The Journal's web site is located at http://intl-ajpcell.physiology.org/
dc.publisher.place	United States
dc.relation.ispartof	American Journal of Physiology - Cell Physiology
dc.relation.references	References in Scopus
dc.subject.mesh	Adenylate Cyclase - Physiology
dc.subject.mesh	Animals
dc.subject.mesh	Anoxia - Physiopathology
dc.subject.mesh	Calcium - Metabolism
dc.subject.mesh	Cardiotonic Agents - Pharmacology
dc.subject.mesh	Cholera Toxin - Pharmacology
dc.subject.mesh	Chronic Disease
dc.subject.mesh	Cyclic Amp - Metabolism
dc.subject.mesh	Electric Stimulation
dc.subject.mesh	Forskolin - Pharmacology
dc.subject.mesh	Gtp-Binding Protein Alpha Subunits, Gs - Physiology
dc.subject.mesh	Heart Ventricles
dc.subject.mesh	Intracellular Membranes - Metabolism
dc.subject.mesh	Isoproterenol - Pharmacology
dc.subject.mesh	Male
dc.subject.mesh	Myocardium - Metabolism - Pathology
dc.subject.mesh	Protein Isoforms - Physiology
dc.subject.mesh	Rats
dc.subject.mesh	Rats, Sprague-Dawley
dc.subject.mesh	Receptors, Adrenergic, Beta - Metabolism
dc.subject.mesh	Reference Values
dc.subject.mesh	Sodium Fluoride - Pharmacology
dc.subject	Cardiac hypertrophy
dc.subject	G protein
dc.title	Impaired G(s)α and adenylyl cyclase cause β-adrenoceptor desensitization in chronically hypoxic rat hearts
dc.type	Article

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Author Affiliations

The University of Hong Kong