Role of CaMKII in RyR leak, EC coupling and action potential duration: a computational model.

ABSTRACT: During heart failure, the ability of the sarcoplasmic reticulum (SR) to store Ca(2+) is severely impaired resulting in abnormal Ca(2+) cycling and excitation-contraction (EC) coupling. Recently, it has been proposed that "leaky" ryanodine receptors (RyRs) contribute to diminished Ca(2+) levels in the SR. Various groups have experimentally investigated the effects of RyR phosphorylation mediated by Ca(2+)/calmodulin-dependent kinase II (CaMKII) on RyR behavior. Some of these results are difficult to interpret since RyR gating is modulated by many external proteins and ions, including Ca(2+). Here, we present a mathematical model representing CaMKII-RyR interaction in the canine ventricular myocyte. This is an extension of our previous model which characterized CaMKII phosphorylation of L-ty

SUBMITTER: Hashambhoy YL 

PROVIDER: S-EPMC2932814 | biostudies-literature | 2010 Oct

REPOSITORIES: biostudies-literature