Linked Life Data

9647487

Source:http://linkedlifedata.com/resource/pubmed/id/9647487

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1998-9-16
pubmed:abstractText
1. The role of protein kinase C (PKC) in mediating the action of kappa-receptor stimulation on intracellular Ca2+ and cyclic AMP production was determined by studying the effects of trans-(+/-)-3,4-dichloro-N-methyl-N-(2-[1-pyrrolidinyl] cyclohexyl) benzeneacetamide methanesulphonate (U50,488H), a selective kappa-receptor agonist, and phorbol 12-myristate 13-acetate (PMA), a PKC agonist, on the electrically-induced [Ca2+]i transient and forskolin-stimulated cyclic AMP accumulation in the presence and absence of a PKC antagonist, staurosporine or chelerythrine, in the single rat ventricular myocyte. 2. U50,488H at 2.5-40 microM decreased both the electrically-induced [Ca2+]i transient and forskolin-stimulated cyclic AMP accumulation dose-dependently, effects which PMA mimicked. The effects of the kappa-agonist, that were blocked by a selective kappa-antagonist, nor-binaltorphimine, were significantly antagonized by the PKC antagonists, staurosporine and/or chelerythrine. The results indicate that PKC mediates the actions of kappa-receptor stimulation. 3. To determine whether the action of PKC was at the sarcoplasmic reticulum (SR) or not, the [Ca2+]i transient induced by caffeine, that depletes the SR of Ca2+, was used as an indicator of Ca2+ content in the SR. The caffeine-induced [Ca2+]i transient was significantly reduced by U50,488H at 20 microM. This effect of U50,488H on caffeine-induced [Ca2+]i transient was significantly attenuated by 1 microM chelerythrine, indicating that the action of PKC involves mobilization of Ca2+ from the SR. When the increase in IP3 production in response to K-receptor stimulation with U50,488H in the ventricular myocyte was determined, the effect of U50,488H was the same in the presence and absence of staurosporine, suggesting that the effect of PKC activation subsequent to kappa-receptor stimulation does not involve IP3. The observations suggest that PKC may act directly at the SR. 4. In conclusion, the present study has provided evidence for the first time that PKC may be involved in the action of kappa-receptor stimulation on Ca2+ in the SR and cyclic AMP production, both of which play an essential role in Ca2+ homeostasis in the heart.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0007-1188
pubmed:author
pubmed:issnType
Print
pubmed:volume
124
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
600-6
pubmed:dateRevised
2008-11-20
pubmed:meshHeading
pubmed-meshheading:9647487-3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benz..., pubmed-meshheading:9647487-Animals, pubmed-meshheading:9647487-Calcium, pubmed-meshheading:9647487-Cyclic AMP, pubmed-meshheading:9647487-Electric Stimulation, pubmed-meshheading:9647487-Enzyme Inhibitors, pubmed-meshheading:9647487-Heart, pubmed-meshheading:9647487-Inosine Triphosphate, pubmed-meshheading:9647487-Male, pubmed-meshheading:9647487-Myocardium, pubmed-meshheading:9647487-Protein Kinase C, pubmed-meshheading:9647487-Rats, pubmed-meshheading:9647487-Rats, Sprague-Dawley, pubmed-meshheading:9647487-Receptors, Opioid, kappa, pubmed-meshheading:9647487-Sarcoplasmic Reticulum, pubmed-meshheading:9647487-Staurosporine, pubmed-meshheading:9647487-Stimulation, Chemical, pubmed-meshheading:9647487-Tetradecanoylphorbol Acetate
pubmed:year
1998
pubmed:articleTitle
Effects of kappa-opioid receptor stimulation in the heart and the involvement of protein kinase C.
pubmed:affiliation
Department of Physiology, Institute of Cardiovascular Science and Medicine, Faculty of Medicine, The University of Hong Kong, China.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't