Synchrony of cardiomyocyte Ca(2+) release is controlled by T-tubule organization, SR Ca(2+) content, and ryanodine receptor Ca(2+) sensitivity.

ABSTRACT: Recent work has demonstrated that cardiomyocyte Ca(2+)release is desynchronized in several pathological conditions. Loss of Ca(2+) release synchrony has been attributed to t-tubule disruption, but it is unknown if other factors also contribute. We investigated this issue in normal and failing myocytes by integrating experimental data with a mathematical model describing spatiotemporal dynamics of Ca(2+) in the cytosol and sarcoplasmic reticulum (SR). Heart failure development in postinfarction mice was associated with progressive t-tubule disorganization, as quantified by fast-Fourier transforms. Data from fast-Fourier transforms were then incorporated in the model as a dyadic organization index, reflecting the proportion of ryanodine receptors located in dyads. With decreasing dyadic-orga

SUBMITTER: Oyehaug L 

PROVIDER: S-EPMC3627865 | biostudies-literature | 2013 Apr

REPOSITORIES: biostudies-literature