Key result
Spontaneous release of calcium in overloaded rat ventricular myocytes effectively activates Ca2+ efflux and minimizes increases in diastolic tension, despite being potentially arrhythmogenic.
Population
Isolated rat ventricular myocytes loaded with the Ca(2+)-sensitive fluorescent indicator indo-1
Comparison
Raising external calcium concentration and… vs Baseline/lower external calcium concentration or…
Design
Preclinical
Authors
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Highlights potential protective role of spontaneous Ca2+ release against diastolic dysfunction; leaves open translation to human HF therapies.
Spontaneous release of calcium in overloaded conditions is an effective mechanism to activate Ca2+ efflux and minimize increases in diastolic tension, despite being potentially arrhythmogenic.
Díaz et al. (1997) studied Calcium overload in ventricular myocytes. Raising external calcium concentration ([Ca2+]o) and inhibiting spontaneous SR Ca2+ release vs. Baseline/quiescent cells was evaluated on Sarcoplasmic reticulum Ca2+ content and sarcolemmal Ca2+ fluxes. Spontaneous release of calcium in overloaded rat ventricular myocytes effectively activates Ca2+ efflux and minimizes increases in diastolic tension, despite being potentially arrhythmogenic.
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