High intracellular calcium concentration causes a transient inward
current (I
n) that can provoke delayed after-depolarizations
(DAD). I
n is comprised of sodium-calcium exchange current (I
NaCa) and calcium-activated chloride current
(I
ClCa). We have developed a mathematical model of I<sub>ClCa
</sub> that was included into the atrium AP model by
... [Show full abstract] Linblad, Murphey,
Clark and Giles (1996) (LMCG model). IClCa appears as an
important component (30-40%) of In. The plots of DAD
amplitudes and DAD higher slope as a function of extracellular Ca<sup>2+
</sup> concentration show an interval between 5 mM/l to 6 mM/l in which
IClCa blockade could bring the DAD amplitude to a
subthreshold level for triggered action potentials. Our results suggest
that, at a high intracellular Ca2+ concentration, that
provokes DAD generating conditions, IClCa blockade could be
potentially antiarrythmogenic
