Key result
Aconitine significantly increased L-type Ca2+ current density from 12.77 to 18.98 pA/pF and induced triggered activities and delayed after-depolarizations in rat ventricular myocytes.
Why the study?
Does aconitine alter intracellular Ca2+ signals to induce arrhythmogenesis in rat ventricular myocytes?
Population
Pathogen-free Sprague-Dawley male adult rats weighing 200-250 g and primary cultures of neonatal rat cardiac…
Comparison
Aconitine (1 µM, 5 µM, and 10 µM) vs Control (no aconitine)
Design
Preclinical
Authors
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Does not warrant clinical practice changes; leaves open Ca2+-dependent arrhythmogenic mechanisms for translational validation.
Does aconitine alter intracellular Ca2+ signals to induce arrhythmogenesis in rat ventricular myocytes?
Absolute Event Rate: 18.98% vs 12.77%
p-value: p=<0.01
Aconitine induces arrhythmogenesis by increasing cytosolic Ca2+ through accelerated L-type Ca2+ currents and altered expression of NCX and SERCA2a, leading to triggered activities and delayed after-depolarizations.
Zhou et al. (2013) studied Arrhythmia (in vitro/animal model). Aconitine vs. Control (untreated cells) was evaluated on L-type Ca2+ current (ICa-L) density (pA/pF) (p=<0.01). Aconitine significantly increased L-type Ca2+ current density from 12.77 to 18.98 pA/pF and induced triggered activities and delayed after-depolarizations in rat ventricular myocytes.
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