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Article: Gs and Gi coupling of adrenomedullin in adult rat ventricular myocytes

TitleGs and Gi coupling of adrenomedullin in adult rat ventricular myocytes
Authors
KeywordsAdenosine 3′5′-cyclic monophosphate-dependent protein kinase inhibitor
Calcium transient
Cell shortening
Pertussis toxin
Septic shock
Issue Date2006
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, 2006, v. 290 n. 5, p. H1842-H1847 How to Cite?
AbstractAdrenomedullin (ADM) acts as an autocrine or a paracrine factor in the regulation of cardiac function. The intracellular mechanisms involved in the direct effect of ADM on adult rat ventricular myocytes (ARVMs) are still to be elucidated. In ARVMs from normal rats, ADM produced an initial (<30 min) increase in cell shortening and Ca2+ transients and a marked decrease in both on prolonged incubation (>1 h). Both effects were sensitive to ADM antagonist ADM-(22-52). Treatment with SQ-22536, an inhibitor of adenylate cyclase, blocked the positive inotropic effect of ADM and potentiated its negative inotropic effect. The negative inotropic effect was sensitive to inhibition by pertussis toxin (PTX), an inhibitor of Gi proteins and KT-5720, an inhibitor of PKA. The observations suggest a switch from G s-coupled to PTX-sensitive, PKA-dependent Gi coupling by ADM in ARVMs. The ADM-mediated Gi-signaling system involves cAMP-dependent pathways because SQ-22536 further increased the negative inotropic actions of ADM. Also, because ADM is overproduced by ARVMs in our rat model of septic shock, ARVMs from LPS-treated rats were subjected to treatment with ADM-(22-52) and PTX. The decrease in cell shortening and Ca2+ transients in LPS-treated ARVMs could be reversed back with ADM-(22-52) and PTX. This indicates that ADM plays a role in mediating the negative inotropic effect in LPS-treated ARVM through the activation of Gi signaling. This study delineates the intracellular pathways involved in ADM-mediated direct inotropic effects on ARVMs and also suggests a role of ADM in sepsis. Copyright © 2006 the American Physiological Society.
Persistent Identifierhttp://hdl.handle.net/10722/81301
ISSN
2015 Impact Factor: 3.324
2015 SCImago Journal Rankings: 1.823
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMittra, Sen_HK
dc.contributor.authorBourreau, JPen_HK
dc.date.accessioned2010-09-06T08:16:06Z-
dc.date.available2010-09-06T08:16:06Z-
dc.date.issued2006en_HK
dc.identifier.citationAmerican Journal Of Physiology - Heart And Circulatory Physiology, 2006, v. 290 n. 5, p. H1842-H1847en_HK
dc.identifier.issn0363-6135en_HK
dc.identifier.urihttp://hdl.handle.net/10722/81301-
dc.description.abstractAdrenomedullin (ADM) acts as an autocrine or a paracrine factor in the regulation of cardiac function. The intracellular mechanisms involved in the direct effect of ADM on adult rat ventricular myocytes (ARVMs) are still to be elucidated. In ARVMs from normal rats, ADM produced an initial (<30 min) increase in cell shortening and Ca2+ transients and a marked decrease in both on prolonged incubation (>1 h). Both effects were sensitive to ADM antagonist ADM-(22-52). Treatment with SQ-22536, an inhibitor of adenylate cyclase, blocked the positive inotropic effect of ADM and potentiated its negative inotropic effect. The negative inotropic effect was sensitive to inhibition by pertussis toxin (PTX), an inhibitor of Gi proteins and KT-5720, an inhibitor of PKA. The observations suggest a switch from G s-coupled to PTX-sensitive, PKA-dependent Gi coupling by ADM in ARVMs. The ADM-mediated Gi-signaling system involves cAMP-dependent pathways because SQ-22536 further increased the negative inotropic actions of ADM. Also, because ADM is overproduced by ARVMs in our rat model of septic shock, ARVMs from LPS-treated rats were subjected to treatment with ADM-(22-52) and PTX. The decrease in cell shortening and Ca2+ transients in LPS-treated ARVMs could be reversed back with ADM-(22-52) and PTX. This indicates that ADM plays a role in mediating the negative inotropic effect in LPS-treated ARVM through the activation of Gi signaling. This study delineates the intracellular pathways involved in ADM-mediated direct inotropic effects on ARVMs and also suggests a role of ADM in sepsis. Copyright © 2006 the American Physiological Society.en_HK
dc.languageengen_HK
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/en_HK
dc.relation.ispartofAmerican Journal of Physiology - Heart and Circulatory Physiologyen_HK
dc.subjectAdenosine 3′5′-cyclic monophosphate-dependent protein kinase inhibitoren_HK
dc.subjectCalcium transienten_HK
dc.subjectCell shorteningen_HK
dc.subjectPertussis toxinen_HK
dc.subjectSeptic shocken_HK
dc.titleGs and Gi coupling of adrenomedullin in adult rat ventricular myocytesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0363-6135&volume=290&spage=H1842&epage=H1847&date=2006&atitle=Gs+And+Gi+Coupling+Of+Adrenomedullin+In+Adult+Rat+Ventricular+Myocytesen_HK
dc.identifier.emailBourreau, JP: bourreau@hkucc.hku.hken_HK
dc.identifier.authorityBourreau, JP=rp00389en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1152/ajpheart.00388.2005en_HK
dc.identifier.pmid16327020en_HK
dc.identifier.scopuseid_2-s2.0-33646394319en_HK
dc.identifier.hkuros116653en_HK
dc.identifier.hkuros113220-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33646394319&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume290en_HK
dc.identifier.issue5en_HK
dc.identifier.spageH1842en_HK
dc.identifier.epageH1847en_HK
dc.identifier.eissn1522-1539-
dc.identifier.isiWOS:000236664900018-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridMittra, S=36725463300en_HK
dc.identifier.scopusauthoridBourreau, JP=7003927886en_HK

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