Document Detail

CaMKII is responsible for activity-dependent acceleration of relaxation in rat ventricular myocytes.
MedLine Citation:
PMID:  7864197     Owner:  NLM     Status:  MEDLINE    
We investigated the role of Ca/calmodulin-dependent protein kinase (CaMKII) in relaxation and cytosolic free [Ca] ([Ca]i) decline during steady-state (SS) and postrest (PR) twitches in intact rat ventricular myocytes. Half-time of mechanical relaxation and time constant of [Ca]i decline (tau) were twofold greater during PR than with SS at 1 Hz. This difference was 1) abolished by inhibition of sarcoplasmic reticulum (SR) Ca accumulation by thapsigargin or caffeine; 2) greater at higher stimulation frequency and extracellular [Ca], which affected only SS tau; 3) abolished by the protein phosphatase inhibitor okadaic acid (10 microM, which selectively accelerated [Ca]i decline during PR); 4) still present during stimulation or inhibition of adenosine 3',5'-cyclic monophosphate-dependent protein kinase (PKA) by 10 microM forskolin or 1 microM H-89, respectively (SS and PR tau values were abbreviated and prolonged, respectively); and 5) suppressed by 10 microM KN-62, a selective inhibitor of CaMKII, which selectively prolonged [Ca]i decline during SS twitches. Both protein kinase inhibitors were also shown to decrease the SR Ca-uptake rate in digitonin-permeabilized rat myocytes. We conclude that CaMKII plays a major role in modulation of relaxation in rat ventricular myocytes, enhancing SR Ca uptake in a activity-dependent fashion. Our results are also compatible with a background, activity-independent stimulation of SR Ca uptake by PKA in intact rat myocytes.
R A Bassani; A Mattiazzi; D M Bers
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The American journal of physiology     Volume:  268     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1995 Feb 
Date Detail:
Created Date:  1995-03-20     Completed Date:  1995-03-20     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  H703-12     Citation Subset:  IM    
Department of Physiology, Loyola University School of Medicine, Maywood, Illinois 60153.
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MeSH Terms
Calcium / metabolism
Calcium-Calmodulin-Dependent Protein Kinases / antagonists & inhibitors,  physiology*
Electric Stimulation
Intracellular Membranes / metabolism
Myocardial Contraction / physiology*
Myocardium / cytology
Osmolar Concentration
Rats, Sprague-Dawley
Sarcoplasmic Reticulum / metabolism
Stimulation, Chemical
Ventricular Function / physiology*
Grant Support
Reg. No./Substance:
7440-70-2/Calcium; EC Protein Kinases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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