Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2003-8-13
pubmed:abstractText
Activation of myocardial kappa-opioid receptor-protein kinase C (PKC) pathways may improve postischemic contractile function through a myofilament reduction in ATP utilization. To test this, we first examined the effects of PKC inhibitors on kappa-opioid receptor-dependent cardioprotection. The kappa-opioid receptor agonist U50,488H (U50) increased postischemic left ventricular developed pressure and reduced postischemic end-diastolic pressure compared with controls. PKC inhibitors abolished the cardioprotective effects of U50. To determine whether kappa-opioid-PKC-dependent decreases in Ca2+-dependent actomyosin Mg2+-ATPase could account for cardioprotection, we subjected hearts to three separate actomyosin ATPase-lowering protocols. We observed that moderate decreases in myofibrillar ATPase were equally cardioprotective as kappa-opioid receptor stimulation. Immunoblot analysis and confocal microscopy revealed a kappa-opioid-induced increase in myofilament-associated PKC-epsilon, and myofibrillar Ca2+-independent PKC activity was increased after kappa-opioid stimulation. This PKC-myofilament association led to an increase in troponin I and C-protein phosphorylation. Thus we propose PKC-epsilon activation and translocation to the myofilaments causes a decrease in actomyosin ATPase, which contributes to the kappa-opioid receptor-dependent cardioprotective mechanism.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0363-6135
pubmed:author
pubmed:issnType
Print
pubmed:volume
285
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H1220-8
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:12763745-3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-ben..., pubmed-meshheading:12763745-Actin Cytoskeleton, pubmed-meshheading:12763745-Adenosine Triphosphatases, pubmed-meshheading:12763745-Adenosine Triphosphate, pubmed-meshheading:12763745-Analgesics, Non-Narcotic, pubmed-meshheading:12763745-Animals, pubmed-meshheading:12763745-Cardiotonic Agents, pubmed-meshheading:12763745-Female, pubmed-meshheading:12763745-Ischemic Preconditioning, Myocardial, pubmed-meshheading:12763745-Isoenzymes, pubmed-meshheading:12763745-Myocardial Ischemia, pubmed-meshheading:12763745-Phosphorylation, pubmed-meshheading:12763745-Protein Kinase C, pubmed-meshheading:12763745-Protein Kinase C-epsilon, pubmed-meshheading:12763745-Rats, pubmed-meshheading:12763745-Rats, Wistar, pubmed-meshheading:12763745-Receptors, Opioid, kappa, pubmed-meshheading:12763745-Ventricular Pressure
pubmed:year
2003
pubmed:articleTitle
Cardioprotection through a PKC-dependent decrease in myofilament ATPase.
pubmed:affiliation
Department of Physiology, University of Tennessee-Memphis, 894 Union Avenue, Memphis, TN 38163, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't