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Article: G(i)-dependent suppression of β1-adrenoceptor effects in ventricular myocytes from NE-treated guinea pigs

TitleG(i)-dependent suppression of β1-adrenoceptor effects in ventricular myocytes from NE-treated guinea pigs
Authors
Issue Date2000
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/
Citation
American Journal Of Physiology - Heart And Circulatory Physiology, 2000, v. 278 n. 6 47-6, p. H1807-H1814 How to Cite?
AbstractIt has been suggested that there is a preferential coupling in heart muscle between the inhibitory G protein (G(i)) and the β2-subtype of the β-adrenergic receptor (β-AR), since pertussis toxin (which inactivates G(i)) reveals latent β2-ARs in rat and mouse myocytes. We have previously shown that guinea pigs treated with norepinephrine (NE) for 7 days have myocytes that are desensitized to β-AR-agonist stimulation, and that pertussis toxin restores these responses. The purpose of the present investigation was to determine whether pertussis toxin specifically upregulated β2-ARs in myocytes from NE-treated guinea pigs. The sole β-AR subtype in control guinea pig myocytes was confirmed as β1-AR by radioligand binding, single-cell autoradiography, and concentration-response curves to isoproterenol in contracting myocytes. In contrast, a minor pool of β2-ARs was observed in rat myocytes by use of the same methods. NE treatment decreased the maximum isoproterenol response (relative to high Ca2+) from 0.89 ± 0.06 to 0.58 ± 0.08 (n = 7, P < 0.01) and the pD2 (- log EC50) from 8.8 ± 0.2 to 7.5 ± 0.2 (n = 7, P < 0.01). Pertussis toxin treatment increased the isoproterenol-to-Ca2+ ratio to 0.88 ± 0.04 (n = 6, P < 0.05) and the pD2 to 8.6 ± 0.3 (P < 0.01). This was not mediated by increases in either number or function of β2-ARs. G(i) is therefore able to modulate β1-AR responses in guinea pig myocytes.
Persistent Identifierhttp://hdl.handle.net/10722/162398
ISSN
2015 Impact Factor: 3.324
2015 SCImago Journal Rankings: 1.823
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorRanu, HKen_US
dc.contributor.authorMak, JCWen_US
dc.contributor.authorBarnes, PJen_US
dc.contributor.authorHarding, SEen_US
dc.date.accessioned2012-09-05T05:19:35Z-
dc.date.available2012-09-05T05:19:35Z-
dc.date.issued2000en_US
dc.identifier.citationAmerican Journal Of Physiology - Heart And Circulatory Physiology, 2000, v. 278 n. 6 47-6, p. H1807-H1814en_US
dc.identifier.issn0363-6135en_US
dc.identifier.urihttp://hdl.handle.net/10722/162398-
dc.description.abstractIt has been suggested that there is a preferential coupling in heart muscle between the inhibitory G protein (G(i)) and the β2-subtype of the β-adrenergic receptor (β-AR), since pertussis toxin (which inactivates G(i)) reveals latent β2-ARs in rat and mouse myocytes. We have previously shown that guinea pigs treated with norepinephrine (NE) for 7 days have myocytes that are desensitized to β-AR-agonist stimulation, and that pertussis toxin restores these responses. The purpose of the present investigation was to determine whether pertussis toxin specifically upregulated β2-ARs in myocytes from NE-treated guinea pigs. The sole β-AR subtype in control guinea pig myocytes was confirmed as β1-AR by radioligand binding, single-cell autoradiography, and concentration-response curves to isoproterenol in contracting myocytes. In contrast, a minor pool of β2-ARs was observed in rat myocytes by use of the same methods. NE treatment decreased the maximum isoproterenol response (relative to high Ca2+) from 0.89 ± 0.06 to 0.58 ± 0.08 (n = 7, P < 0.01) and the pD2 (- log EC50) from 8.8 ± 0.2 to 7.5 ± 0.2 (n = 7, P < 0.01). Pertussis toxin treatment increased the isoproterenol-to-Ca2+ ratio to 0.88 ± 0.04 (n = 6, P < 0.05) and the pD2 to 8.6 ± 0.3 (P < 0.01). This was not mediated by increases in either number or function of β2-ARs. G(i) is therefore able to modulate β1-AR responses in guinea pig myocytes.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Heart and Circulatory Physiologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAutoradiographyen_US
dc.subject.meshBinding, Competitiveen_US
dc.subject.meshGtp-Binding Protein Alpha Subunits, Gi-Go - Physiologyen_US
dc.subject.meshGuinea Pigsen_US
dc.subject.meshHeart - Drug Effectsen_US
dc.subject.meshLigandsen_US
dc.subject.meshMaleen_US
dc.subject.meshMyocardial Contractionen_US
dc.subject.meshMyocardium - Cytology - Metabolismen_US
dc.subject.meshNorepinephrine - Pharmacologyen_US
dc.subject.meshPertussis Toxinen_US
dc.subject.meshReceptors, Adrenergic, Beta - Drug Effects - Metabolism - Physiologyen_US
dc.subject.meshUp-Regulationen_US
dc.subject.meshVirulence Factors, Bordetella - Pharmacologyen_US
dc.titleG(i)-dependent suppression of β1-adrenoceptor effects in ventricular myocytes from NE-treated guinea pigsen_US
dc.typeArticleen_US
dc.identifier.emailMak, JCW:judymak@hku.hken_US
dc.identifier.authorityMak, JCW=rp00352en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid10843876-
dc.identifier.scopuseid_2-s2.0-0033921994en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033921994&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume278en_US
dc.identifier.issue6 47-6en_US
dc.identifier.spageH1807en_US
dc.identifier.epageH1814en_US
dc.identifier.isiWOS:000087573500011-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridRanu, HK=7004169594en_US
dc.identifier.scopusauthoridMak, JCW=7103323094en_US
dc.identifier.scopusauthoridBarnes, PJ=36064679400en_US
dc.identifier.scopusauthoridHarding, SE=7202447604en_US

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