Abstract
The mechanisms underlying many important properties of the human atrial
action potential (AP) are poorly understood. Using specific formulations
of the K$^+$, Na$^+$, and Ca$^2+$ currents based on data
recorded from human atrial myocytes, along with representations of
pump, exchange, and background currents, we developed a mathematical
model of the AP. The model AP resembles APs recorded from human atrial
samples and responds to rate changes, L-type Ca$^2+$ current
blockade, Na$^+$/Ca$^2+$ exchanger inhibition, and variations
in transient outward current amplitude in a fashion similar to experimental
recordings. Rate-dependent adaptation of AP duration, an important
determinant of susceptibility to atrial fibrillation, was attributable
to incomplete L-type Ca$^2+$ current recovery from inactivation
and incomplete delayed rectifier current deactivation at rapid rates.
Experimental observations of variable AP morphology could be accounted
for by changes in transient outward current density, as suggested
experimentally. We conclude that this mathematical model of the human
atrial AP reproduces a variety of observed AP behaviors and provides
insights into the mechanisms of clinically important AP properties.
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