Journal
BIOPHYSICAL JOURNAL
Volume 91, Issue 1, Pages 95-112Publisher
CELL PRESS
DOI: 10.1529/biophysj.105.077214
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Funding
- NHLBI NIH HHS [R01HL50435-05, K25 HL068704, R01HL071865, R01 HL071865, K25HL068704, R01HL68733, R01 HL068733] Funding Source: Medline
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Spontaneously generated calcium (Ca2+) waves can trigger arrhythmias in ventricular and atrial myocytes. Yet, Ca2+ waves also serve the physiological function of mediating global Ca2+ increase and muscle contraction in atrial myocytes. We examine the factors that influence Ca2+ wave initiation by mathematical modeling and large-scale computational (supercomputer) simulations. An important finding is the existence of a strong coupling between the ryanodine receptor distribution and Ca2+ dynamics. Even modest changes in the ryanodine receptor spacing profoundly affect the probability of Ca2+ wave initiation. As a consequence of this finding, we suggest that there is information flow from the contractile system to the Ca2+ control system and this dynamical interplay could contribute to the increased incidence of arrhythmias during heart failure.
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