Enhanced Ca 2+ Release and Na/Ca Exchange Activity in Hypertrophied Canine Ventricular Myocytes
Authors
Discussion
Loading...
Member takes
Implication
Hypothesis-generating for calcium-driven arrhythmias in hypertrophy; requires human validation before any clinical relevance.
Key Points
- To determine whether alterations in calcium homeostasis support contractile adaptation and contribute to ventricular arrhythmogenesis in a canine model of chronic complete atrioventricular block.
- Isolated ventricular myocytes enzymatically from a canine model with chronic complete atrioventricular block and biventricular hypertrophy.
- Measured myocyte shortening, sarcoplasmic reticulum calcium release and content, L-type calcium currents, and sodium-calcium exchange activity across stimulation frequencies.
- Cell shortening, sarcoplasmic reticulum calcium release, and sarcoplasmic reticulum calcium content were elevated at low stimulation frequencies.
- Calcium influx and inward electrical currents via the sodium-calcium exchanger were significantly increased, while L-type calcium channel currents remained unchanged.
- Alterations in calcium flux were more pronounced in the left ventricle than in the right ventricle.
Cite This Study
Sipido et al. (2000) studied this question.