Abstract
The multifunctional Ca2+/calmodulin-dependent protein kinase (CaMKII) is an enzyme whose regulatory role in the heart is well documented. Despite its known action on a wide range of intracellular targets, the functional role of CaMKII in cardiac myocytes has yet to be fully determined. Due to its potential importance in cell rate dependence and arrhythmogenesis, we integrate dynamic CaMKII activity into a new mathematical model of the canine ventricular myocyte. We use the model to investigate the ionic mechanisms underlying dependence of the Ca2+ transient (CaT) and action potential duration (APD) on pacing rate. Computer simulations identify the importance of the L-type Ca2+ current and CaMKII to the normal rate dependence of APD and the CaT. Our results suggest that suppression of CaMKII activity may be an important component of the remodeling process in myocardial infarction.
| Original language | English |
|---|---|
| Pages (from-to) | 7-8 |
| Number of pages | 2 |
| Journal | Annual International Conference of the IEEE Engineering in Medicine and Biology - Proceedings |
| Volume | 1 |
| State | Published - 2003 |
| Event | A New Beginning for Human Health: Proceedings of the 25th Annual International Conference of the IEEE Engineering in Medicine and Biology Society - Cancun, Mexico Duration: Sep 17 2003 → Sep 21 2003 |
Keywords
- Action potential
- Calcium transient
- Cardiac cell model