Key result
Internal palmitoylcarnitine reduces transient outward K+ current density by ~62% in rat ventricular myocytes.
Why the study?
Fatty acid metabolites accumulate in the heart under pathophysiological conditions and can cause electrophysiological changes that are arrhythmogenic, but their impact on cardiac K+ currents is unclear.
Population
Rat ventricular myocytes
Comparison
Internal dialysis with palmitoylcarnitine or palmitoyl-CoA vs control and other metabolite exposures
Design
Preclinical whole cell voltage-clamp study
Authors
Loading...
Amphiphilic metabolites may inhibit Ito in myocytes; hypothesis-generating for arrhythmogenesis in ischemia or diabetes.
p-value: p=< 0.05
Amphiphilic fatty acid metabolites downregulate transient outward K+ channels from the cytoplasmic side, which may contribute to arrhythmogenesis in conditions like ischemia or diabetes.
Zhi et al. (1998) studied this question. Palmitoylcarnitine and palmitoyl-CoA vs. Control was evaluated on Transient outward (Ito) K+ current density (p=< 0.05). Internal dialysis with 10 microM palmitoylcarnitine or palmitoyl-CoA reduced mean transient outward K+ current density in rat ventricular myocytes by 62% and 37%, respectively (P < 0.05).