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Article: Impaired [Ca2+](i) and pH(i) responses to κ-opioid receptor stimulation in the heart of chronically hypoxic rats
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TitleImpaired [Ca2+](i) and pH(i) responses to κ-opioid receptor stimulation in the heart of chronically hypoxic rats
 
AuthorsPei, JM1
Zhou, JJ1
Bian, JS1
Yu, XC1
Fung, ML1
Wong, TM1
 
Issue Date2000
 
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpcell.physiology.org/
 
CitationAmerican 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.
 
ISSN0363-6143
2013 Impact Factor: 3.674
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorPei, JM
 
dc.contributor.authorZhou, JJ
 
dc.contributor.authorBian, JS
 
dc.contributor.authorYu, XC
 
dc.contributor.authorFung, ML
 
dc.contributor.authorWong, TM
 
dc.date.accessioned2012-10-30T06:16:17Z
 
dc.date.available2012-10-30T06:16:17Z
 
dc.date.issued2000
 
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.
 
dc.description.naturelink_to_subscribed_fulltext
 
dc.identifier.citationAmerican Journal Of Physiology - Cell Physiology, 2000, v. 279 n. 5 48-5, p. C1483-C1494 [How to Cite?]
 
dc.identifier.epageC1494
 
dc.identifier.hkuros59996
 
dc.identifier.issn0363-6143
2013 Impact Factor: 3.674
 
dc.identifier.issue5 48-5
 
dc.identifier.pmid11029296
 
dc.identifier.scopuseid_2-s2.0-0033715773
 
dc.identifier.spageC1483
 
dc.identifier.urihttp://hdl.handle.net/10722/171675
 
dc.identifier.volume279
 
dc.languageeng
 
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpcell.physiology.org/
 
dc.publisher.placeUnited States
 
dc.relation.ispartofAmerican Journal of Physiology - Cell Physiology
 
dc.relation.referencesReferences in Scopus
 
dc.subject.mesh3,4-Dichloro-N-Methyl-N-(2-(1-Pyrrolidinyl)-Cyclohexyl)-Benzeneacetamide, (Trans)-Isomer - Pharmacology
 
dc.subject.meshAnimals
 
dc.subject.meshAnoxia - Metabolism
 
dc.subject.meshCalcium - Metabolism
 
dc.subject.meshChronic Disease
 
dc.subject.meshElectric Stimulation
 
dc.subject.meshHeart Ventricles
 
dc.subject.meshHydrogen-Ion Concentration
 
dc.subject.meshIntracellular Membranes - Metabolism
 
dc.subject.meshMale
 
dc.subject.meshMyocardial Contraction - Drug Effects
 
dc.subject.meshMyocardium - Metabolism - Pathology
 
dc.subject.meshOsmolar Concentration
 
dc.subject.meshProtons
 
dc.subject.meshRna, Messenger - Metabolism
 
dc.subject.meshRats
 
dc.subject.meshRats, Sprague-Dawley
 
dc.subject.meshReceptors, Opioid, Kappa - Genetics - Metabolism
 
dc.subject.meshTetradecanoylphorbol Acetate - Pharmacology
 
dc.titleImpaired [Ca2+](i) and pH(i) responses to κ-opioid receptor stimulation in the heart of chronically hypoxic rats
 
dc.typeArticle
 
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Author Affiliations
  1. The University of Hong Kong