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Article: Impaired [Ca2+](i) and pH(i) responses to κ-opioid receptor stimulation in the heart of chronically hypoxic rats

TitleImpaired [Ca2+](i) and pH(i) responses to κ-opioid receptor stimulation in the heart of chronically hypoxic rats
Authors
Issue Date2000
PublisherAmerican 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. C1483-C1494 How to Cite?
Abstractκ-Opioid receptor (κ-OR) stimulation with U50,488H, a selective κ-OR agonist, or activation of protein kinase C (PKC) with 4-phorbol 12-myristate 13-acetate (PMA), an activator of PKC, decreased the electrically induced intracellular Ca2+ ([Ca2+](i)) transient and increased the intracellular pH (pH(i)) in single ventricular myocytes of rats subjected to 10% oxygen for 4 wk. The effects of U50,488H were abolished by nor-binaltorphimine, a selective κ-OR antagonist, and calphostin C, a specific inhibitor of PKC, while the effects of PMA were abolished by calphostin C and ethylisopropylamiloride (EIPA), a potent Na+/H+ exchange blocker. In both right hypertrophied and left nonhypertrophied ventricles of chronically hypoxic rats, the effects of U50,488H or PMA on [Ca2+](i) transient and pH(i) were significantly attenuated and completely abolished, respectively. Results are first evidence that the [Ca2+](i) and pH(i) responses to κ-OR stimulation are attenuated in the chronically hypoxic rat heart, which may be due to reduced responses to PKC activation. Responses to all treatments were the same for right and left ventricles, indicating that the functional impairment is independent of hypertrophy. κ-OR mRNA expression was the same in right and left ventricles of both normoxic and hypoxic rats, indicating no regional specificity.
Persistent Identifierhttp://hdl.handle.net/10722/171675
ISSN
2015 Impact Factor: 3.395
2015 SCImago Journal Rankings: 1.893
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorPei, JMen_US
dc.contributor.authorZhou, JJen_US
dc.contributor.authorBian, JSen_US
dc.contributor.authorYu, XCen_US
dc.contributor.authorFung, MLen_US
dc.contributor.authorWong, TMen_US
dc.date.accessioned2012-10-30T06:16:17Z-
dc.date.available2012-10-30T06:16:17Z-
dc.date.issued2000en_US
dc.identifier.citationAmerican Journal Of Physiology - Cell Physiology, 2000, v. 279 n. 5 48-5, p. C1483-C1494en_US
dc.identifier.issn0363-6143en_US
dc.identifier.urihttp://hdl.handle.net/10722/171675-
dc.description.abstractκ-Opioid receptor (κ-OR) stimulation with U50,488H, a selective κ-OR agonist, or activation of protein kinase C (PKC) with 4-phorbol 12-myristate 13-acetate (PMA), an activator of PKC, decreased the electrically induced intracellular Ca2+ ([Ca2+](i)) transient and increased the intracellular pH (pH(i)) in single ventricular myocytes of rats subjected to 10% oxygen for 4 wk. The effects of U50,488H were abolished by nor-binaltorphimine, a selective κ-OR antagonist, and calphostin C, a specific inhibitor of PKC, while the effects of PMA were abolished by calphostin C and ethylisopropylamiloride (EIPA), a potent Na+/H+ exchange blocker. In both right hypertrophied and left nonhypertrophied ventricles of chronically hypoxic rats, the effects of U50,488H or PMA on [Ca2+](i) transient and pH(i) were significantly attenuated and completely abolished, respectively. Results are first evidence that the [Ca2+](i) and pH(i) responses to κ-OR stimulation are attenuated in the chronically hypoxic rat heart, which may be due to reduced responses to PKC activation. Responses to all treatments were the same for right and left ventricles, indicating that the functional impairment is independent of hypertrophy. κ-OR mRNA expression was the same in right and left ventricles of both normoxic and hypoxic rats, indicating no regional specificity.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpcell.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Cell Physiologyen_US
dc.subject.mesh3,4-Dichloro-N-Methyl-N-(2-(1-Pyrrolidinyl)-Cyclohexyl)-Benzeneacetamide, (Trans)-Isomer - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnoxia - Metabolismen_US
dc.subject.meshCalcium - Metabolismen_US
dc.subject.meshChronic Diseaseen_US
dc.subject.meshElectric Stimulationen_US
dc.subject.meshHeart Ventriclesen_US
dc.subject.meshHydrogen-Ion Concentrationen_US
dc.subject.meshIntracellular Membranes - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshMyocardial Contraction - Drug Effectsen_US
dc.subject.meshMyocardium - Metabolism - Pathologyen_US
dc.subject.meshOsmolar Concentrationen_US
dc.subject.meshProtonsen_US
dc.subject.meshRna, Messenger - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshReceptors, Opioid, Kappa - Genetics - Metabolismen_US
dc.subject.meshTetradecanoylphorbol Acetate - Pharmacologyen_US
dc.titleImpaired [Ca2+](i) and pH(i) responses to κ-opioid receptor stimulation in the heart of chronically hypoxic ratsen_US
dc.typeArticleen_US
dc.identifier.emailFung, ML:fungml@hkucc.hku.hken_US
dc.identifier.emailWong, TM: tm.wong@hkuspace.hku.hk-
dc.identifier.authorityFung, ML=rp00433en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid11029296-
dc.identifier.scopuseid_2-s2.0-0033715773en_US
dc.identifier.hkuros59996-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033715773&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume279en_US
dc.identifier.issue5 48-5en_US
dc.identifier.spageC1483en_US
dc.identifier.epageC1494en_US
dc.identifier.isiWOS:000089790300021-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridPei, JM=7103299061en_US
dc.identifier.scopusauthoridZhou, JJ=7405545441en_US
dc.identifier.scopusauthoridBian, JS=7103200001en_US
dc.identifier.scopusauthoridYu, XC=7404114600en_US
dc.identifier.scopusauthoridFung, ML=7101955092en_US
dc.identifier.scopusauthoridWong, TM=7403531434en_US

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