Mechanisms of altered excitation-contraction coupling in canine tachycardia-induced heart failure, II: model studies. Winslow, R., Rice, J., Jafri, S., Marban, E., & O'Rourke, B. j-CR, 84(5):571--586, March, 1999. bibtex @Article{RSM:Win99,
author = "R.L. Winslow and J. Rice and S. Jafri and E. Marban
and B. O'Rourke",
title = "Mechanisms of altered excitation-contraction coupling
in canine tachycardia-induced heart failure, {II}:
model studies.",
journal = j-CR,
year = "1999",
month = mar,
volume = "84",
number = "5",
pages = "571--586",
robnote = "Ca2+ transients measured in failing human ventricular
myocytes exhibit reduced amplitude, slowed relaxation,
and blunted frequency dependence. In the companion
article (O'Rourke B, Kass DA, Tomaselli GF, Kaab S,
Tunin R, Marban E. Mechanisms of altered
excitation-contraction coupling in canine
tachycardia-induced heart, I: experimental studies.
Circ Res. 1999;84:562-570), O'Rourke et al show that
Ca2+ transients recorded in myocytes isolated from
canine hearts subjected to the tachycardia pacing
protocol exhibit similar responses. Analyses of protein
levels in these failing hearts reveal that both SR Ca2+
ATPase and phospholamban are decreased on average by
28\% and that Na+/Ca2+ exchanger (NCX) protein is
increased on average by 104\%. In this article, we
present a model of the canine midmyocardial ventricular
action potential and Ca2+ transient. The model is used
to estimate the degree of functional upregulation and
downregulation of NCX and SR Ca2+ ATPase in heart
failure using data obtained from 2 different
experimental protocols. Model estimates of average SR
Ca2+ ATPase functional downregulation obtained using
these experimental protocols are 49\% and 62\%. Model
estimates of average NCX functional upregulation range
are 38\% and 75\%. Simulation of voltage-clamp Ca2+
transients indicates that such changes are sufficient
to account for the reduced amplitude, altered shape,
and slowed relaxation of Ca2+ transients in the failing
canine heart. Model analyses also suggest that altered
expression of Ca2+ handling proteins plays a
significant role in prolongation of action potential
duration in failing canine myocytes.",
bibdate = "Fri Jul 20 18:14:08 2001",
}
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In the companion article (O'Rourke B, Kass DA, Tomaselli GF, Kaab S, Tunin R, Marban E. Mechanisms of altered excitation-contraction coupling in canine tachycardia-induced heart, I: experimental studies. Circ Res. 1999;84:562-570), O'Rourke et al show that Ca2+ transients recorded in myocytes isolated from canine hearts subjected to the tachycardia pacing protocol exhibit similar responses. Analyses of protein levels in these failing hearts reveal that both SR Ca2+ ATPase and phospholamban are decreased on average by 28% and that Na+/Ca2+ exchanger (NCX) protein is increased on average by 104%. In this article, we present a model of the canine midmyocardial ventricular action potential and Ca2+ transient. The model is used to estimate the degree of functional upregulation and downregulation of NCX and SR Ca2+ ATPase in heart failure using data obtained from 2 different experimental protocols. Model estimates of average SR Ca2+ ATPase functional downregulation obtained using these experimental protocols are 49% and 62%. Model estimates of average NCX functional upregulation range are 38% and 75%. Simulation of voltage-clamp Ca2+ transients indicates that such changes are sufficient to account for the reduced amplitude, altered shape, and slowed relaxation of Ca2+ transients in the failing canine heart. Model analyses also suggest that altered expression of Ca2+ handling proteins plays a significant role in prolongation of action potential duration in failing canine myocytes.","bibdate":"Fri Jul 20 18:14:08 2001","bibtex":"@Article{RSM:Win99,\n author = \"R.L. Winslow and J. Rice and S. Jafri and E. Marban\n and B. O'Rourke\",\n title = \"Mechanisms of altered excitation-contraction coupling\n in canine tachycardia-induced heart failure, {II}:\n model studies.\",\n journal = j-CR,\n year = \"1999\",\n month = mar,\n volume = \"84\",\n number = \"5\",\n pages = \"571--586\",\n robnote = \"Ca2+ transients measured in failing human ventricular\n myocytes exhibit reduced amplitude, slowed relaxation,\n and blunted frequency dependence. In the companion\n article (O'Rourke B, Kass DA, Tomaselli GF, Kaab S,\n Tunin R, Marban E. Mechanisms of altered\n excitation-contraction coupling in canine\n tachycardia-induced heart, I: experimental studies.\n Circ Res. 1999;84:562-570), O'Rourke et al show that\n Ca2+ transients recorded in myocytes isolated from\n canine hearts subjected to the tachycardia pacing\n protocol exhibit similar responses. Analyses of protein\n levels in these failing hearts reveal that both SR Ca2+\n ATPase and phospholamban are decreased on average by\n 28\\% and that Na+/Ca2+ exchanger (NCX) protein is\n increased on average by 104\\%. In this article, we\n present a model of the canine midmyocardial ventricular\n action potential and Ca2+ transient. The model is used\n to estimate the degree of functional upregulation and\n downregulation of NCX and SR Ca2+ ATPase in heart\n failure using data obtained from 2 different\n experimental protocols. Model estimates of average SR\n Ca2+ ATPase functional downregulation obtained using\n these experimental protocols are 49\\% and 62\\%. Model\n estimates of average NCX functional upregulation range\n are 38\\% and 75\\%. Simulation of voltage-clamp Ca2+\n transients indicates that such changes are sufficient\n to account for the reduced amplitude, altered shape,\n and slowed relaxation of Ca2+ transients in the failing\n canine heart. Model analyses also suggest that altered\n expression of Ca2+ handling proteins plays a\n significant role in prolongation of action potential\n duration in failing canine myocytes.\",\n bibdate = \"Fri Jul 20 18:14:08 2001\",\n}\n\n","author_short":["Winslow, R.","Rice, J.","Jafri, S.","Marban, E.","O'Rourke, B."],"key":"RSM:Win99","id":"RSM:Win99","bibbaseid":"winslow-rice-jafri-marban-orourke-mechanismsofalteredexcitationcontractioncouplingincaninetachycardiainducedheartfailureiimodelstudies-1999","role":"author","urls":{},"downloads":0,"html":""},"search_terms":["mechanisms","altered","excitation","contraction","coupling","canine","tachycardia","induced","heart","failure","model","studies","winslow","rice","jafri","marban","o'rourke"],"keywords":[],"authorIDs":[],"dataSources":["5HG3Kp8zRwDd7FotB"]}