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Article: Effect of SIN-1 in rat ventricular myocytes: Interference with β-adrenergic stimulation

TitleEffect of SIN-1 in rat ventricular myocytes: Interference with β-adrenergic stimulation
Authors
Issue Date2002
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescie
Citation
Life Sciences, 2002, v. 71 n. 3, p. 287-297 How to Cite?
AbstractWe have examined the effects of the nitric oxide (NO) donor, 3-morpholino-sydnonimine (SIN-1), on Ca 2+ transients, L-type Ca 2+ current (I Ca,L), and cGMP/cAMP content in electrically-stimulated rat ventricular myocytes in the absence and presence of the β-adrenergic stimulation with isoproterenol. SIN-1 had no effect at low concentrations, but decreased the amplitude of electrically-induced Ca 2+ transients at higher concentrations. SIN-1 attenuated the increase in Ca 2+ transients induced by isoproterenol in a concentration-dependent manner. SIN-1 Also reduced the amplitude of caffeine-induced Ca 2+ transients, and the increase in I Ca,L induced by isoproterenol. These effects of SIN-1 were associated with an increased cGMP and a decreased cAMP content in ventricular myocytes in either the absence or presence of isoproterenol. These data suggest that the inhibitory effect of SIN-1 on basal and β-adrenergic stimulated Ca2+ signal in ventricular myocytes could be due to the depression in the SR function and I Ca,L, possibly mediated by a cGMP/cAMP-dependent mechanism. Taken together, the present study supports the idea that NO acts as an inhibitory modulator of the cardiac function during pathological conditions associated with an abnormal production of NO such as septic shock. © 2002 Published by Elsevier Science Inc.
Persistent Identifierhttp://hdl.handle.net/10722/171708
ISSN
2015 Impact Factor: 2.685
2015 SCImago Journal Rankings: 1.056
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYin, Xen_US
dc.contributor.authorShan, Qen_US
dc.contributor.authorDeng, Cen_US
dc.contributor.authorBourreau, JPen_US
dc.date.accessioned2012-10-30T06:16:31Z-
dc.date.available2012-10-30T06:16:31Z-
dc.date.issued2002en_US
dc.identifier.citationLife Sciences, 2002, v. 71 n. 3, p. 287-297en_US
dc.identifier.issn0024-3205en_US
dc.identifier.urihttp://hdl.handle.net/10722/171708-
dc.description.abstractWe have examined the effects of the nitric oxide (NO) donor, 3-morpholino-sydnonimine (SIN-1), on Ca 2+ transients, L-type Ca 2+ current (I Ca,L), and cGMP/cAMP content in electrically-stimulated rat ventricular myocytes in the absence and presence of the β-adrenergic stimulation with isoproterenol. SIN-1 had no effect at low concentrations, but decreased the amplitude of electrically-induced Ca 2+ transients at higher concentrations. SIN-1 attenuated the increase in Ca 2+ transients induced by isoproterenol in a concentration-dependent manner. SIN-1 Also reduced the amplitude of caffeine-induced Ca 2+ transients, and the increase in I Ca,L induced by isoproterenol. These effects of SIN-1 were associated with an increased cGMP and a decreased cAMP content in ventricular myocytes in either the absence or presence of isoproterenol. These data suggest that the inhibitory effect of SIN-1 on basal and β-adrenergic stimulated Ca2+ signal in ventricular myocytes could be due to the depression in the SR function and I Ca,L, possibly mediated by a cGMP/cAMP-dependent mechanism. Taken together, the present study supports the idea that NO acts as an inhibitory modulator of the cardiac function during pathological conditions associated with an abnormal production of NO such as septic shock. © 2002 Published by Elsevier Science Inc.en_US
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescieen_US
dc.relation.ispartofLife Sciencesen_US
dc.rightsLife Sciences . Copyright © Elsevier Inc.-
dc.subject.meshAnimalsen_US
dc.subject.meshCaffeine - Pharmacologyen_US
dc.subject.meshCalcium - Metabolismen_US
dc.subject.meshCalcium Channels - Drug Effects - Physiologyen_US
dc.subject.meshCyclic Amp - Metabolismen_US
dc.subject.meshCyclic Gmp - Metabolismen_US
dc.subject.meshDrug Interactionsen_US
dc.subject.meshHeart Ventricles - Cytology - Drug Effectsen_US
dc.subject.meshMolsidomine - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshMyocardium - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshReceptors, Adrenergic, Beta - Metabolismen_US
dc.subject.meshVasodilator Agents - Pharmacologyen_US
dc.titleEffect of SIN-1 in rat ventricular myocytes: Interference with β-adrenergic stimulationen_US
dc.typeArticleen_US
dc.identifier.emailBourreau, JP:bourreau@hkucc.hku.hken_US
dc.identifier.authorityBourreau, JP=rp00389en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S0024-3205(02)01625-9en_US
dc.identifier.pmid12034347-
dc.identifier.scopuseid_2-s2.0-0037036158en_US
dc.identifier.hkuros82125-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037036158&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume71en_US
dc.identifier.issue3en_US
dc.identifier.spage287en_US
dc.identifier.epage297en_US
dc.identifier.isiWOS:000176575700004-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridYin, X=55217096200en_US
dc.identifier.scopusauthoridShan, Q=7007145043en_US
dc.identifier.scopusauthoridDeng, C=8689518900en_US
dc.identifier.scopusauthoridBourreau, JP=7003927886en_US

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