This model analyzes the influence of voltage-dependent calcium (Ca2+)-independent transient current (Ito1) on the action potential duration (APD) in normal vs failing canine and human cardiac myocytes.

Description

 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, Marbán 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. 	

Equations

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