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Article: Forskolin fails to activate L-type calcium current in hypertrophied cardiomyocytes of chronically hypoxic rats

TitleForskolin fails to activate L-type calcium current in hypertrophied cardiomyocytes of chronically hypoxic rats
Authors
Keywordsβ-adrenoceptor receptors
Adenylyl cyclase
Calcium current
cAMP
Cardiomyocyte
Chronic hypoxia
Forskolin
Hypertrophy
Issue Date2002
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescie
Citation
Life Sciences, 2002, v. 70 n. 15, p. 1801-1809 How to Cite?
AbstractWe have shown that the contractile, cytosolic calcium ([Ca2+]i) and cyclic AMP (cAMP) responses to β-adrenoceptor stimulation are attenuated in ventricular myocytes of chronically hypoxic (CH) rats. The aim of this study was to examine the effect of forskolin on the L-type Ca2+ current in CH hypertrophied ventricular myocytes. Patch-clamp recording of the L-type Ca2+ current was measured in right ventricular myocytes of normoxic control and CH rats exposed to 10% inspired oxygen for 4 weeks. The breadth, but not the length, of CH myocytes was significantly greater than that of the control group. Activation of β-adrenoceptor with isoproterenol (0.1 μM) increased the peak Ca2+ current by 83% in the normoxic control but the increase of peak Ca2+ current was not significant in the CH myocytes. Forskolin (0.1-1 μM), an activator of adenylyl cyclase, increased the peak Ca2+ current by 49%-102% in the normoxic controls but it did not cause significant change of the peak Ca2+ current in CH myocytes. These results suggest an absence of forskolin-induced activation of Ca2+ current in hypertrophied ventricular myocytes during chronic hypoxia. The failure of activation of the Ca2+ current is consistent with the idea that adenylyl cyclase function is down-regulated in CH hypertrophied myocytes. © 2002 Elsevier Science Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/81342
ISSN
2015 Impact Factor: 2.685
2015 SCImago Journal Rankings: 1.056
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFung, MLen_HK
dc.contributor.authorLi, HYen_HK
dc.contributor.authorWong, TMen_HK
dc.date.accessioned2010-09-06T08:16:33Z-
dc.date.available2010-09-06T08:16:33Z-
dc.date.issued2002en_HK
dc.identifier.citationLife Sciences, 2002, v. 70 n. 15, p. 1801-1809en_HK
dc.identifier.issn0024-3205en_HK
dc.identifier.urihttp://hdl.handle.net/10722/81342-
dc.description.abstractWe have shown that the contractile, cytosolic calcium ([Ca2+]i) and cyclic AMP (cAMP) responses to β-adrenoceptor stimulation are attenuated in ventricular myocytes of chronically hypoxic (CH) rats. The aim of this study was to examine the effect of forskolin on the L-type Ca2+ current in CH hypertrophied ventricular myocytes. Patch-clamp recording of the L-type Ca2+ current was measured in right ventricular myocytes of normoxic control and CH rats exposed to 10% inspired oxygen for 4 weeks. The breadth, but not the length, of CH myocytes was significantly greater than that of the control group. Activation of β-adrenoceptor with isoproterenol (0.1 μM) increased the peak Ca2+ current by 83% in the normoxic control but the increase of peak Ca2+ current was not significant in the CH myocytes. Forskolin (0.1-1 μM), an activator of adenylyl cyclase, increased the peak Ca2+ current by 49%-102% in the normoxic controls but it did not cause significant change of the peak Ca2+ current in CH myocytes. These results suggest an absence of forskolin-induced activation of Ca2+ current in hypertrophied ventricular myocytes during chronic hypoxia. The failure of activation of the Ca2+ current is consistent with the idea that adenylyl cyclase function is down-regulated in CH hypertrophied myocytes. © 2002 Elsevier Science Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescieen_HK
dc.relation.ispartofLife Sciencesen_HK
dc.rightsLife Sciences. Copyright © Elsevier Inc.en_HK
dc.subjectβ-adrenoceptor receptorsen_HK
dc.subjectAdenylyl cyclaseen_HK
dc.subjectCalcium currenten_HK
dc.subjectcAMPen_HK
dc.subjectCardiomyocyteen_HK
dc.subjectChronic hypoxiaen_HK
dc.subjectForskolinen_HK
dc.subjectHypertrophyen_HK
dc.titleForskolin fails to activate L-type calcium current in hypertrophied cardiomyocytes of chronically hypoxic ratsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0024-3205&volume=70 &issue=15&spage=1801&epage=1809&date=2002&atitle=Forskolin+fails+to+activate+L-type+calcium+current+in+hypertrophied+cardiomyocytes+of+chronically+hypoxic+ratsen_HK
dc.identifier.emailFung, ML: fungml@hkucc.hku.hken_HK
dc.identifier.authorityFung, ML=rp00433en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0024-3205(02)01472-8en_HK
dc.identifier.pmid12002524-
dc.identifier.scopuseid_2-s2.0-0036498591en_HK
dc.identifier.hkuros71915en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036498591&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume70en_HK
dc.identifier.issue15en_HK
dc.identifier.spage1801en_HK
dc.identifier.epage1809en_HK
dc.identifier.isiWOS:000174853600008-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridFung, ML=7101955092en_HK
dc.identifier.scopusauthoridLi, HY=8701136400en_HK
dc.identifier.scopusauthoridWong, TM=7403531434en_HK

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