AJP - Heart and Circulatory Physiology, Vol 249, Issue 1 122-H132, Copyright © 1985 by American Physiological Society
Slow inward current may produce many results attributed to IX1 in cardiac Purkinje fibers
J. M. Jaeger and W. R. Gibbons
We have tried to answer two fundamental questions concerning the outward
current IX1 of cardiac Purkinje fibers. 1) Is it possible that current
changes identified as arising from IX1 in voltage-clamp experiments are
actually manifestations of changes in the slow inward current (Isi); and 2)
is IX1 in fact required to produce the electrical phenomena attributed to
it? Isi behavior and the role of IX1 were explored using computer
simulation. The Isi model produced current changes during depolarizations
and hyperpolarizations from depolarized resting potentials like those
attributed to IX1. It also produced a component of "tail currents" that
behaved like IX1. If these current changes were analyzed, assuming that an
outward current is responsible, the resulting kinetics and current voltage
relation would be very similar to the kinetics and current voltage relation
reported for IX1. Using the McAllister, Noble, and Tsien formulation of the
Purkinje fiber action potential, we found that IX1 is not essential for
repolarization of the reconstructed action potential nor is it needed to
reproduce interval duration effects and the effects of applied current in
that model. Data suggesting that calcium channel blockers reduce IX1 and
that catecholamines increase IX1 may be explained as arising from changes
in Isi. Thus many manifestations of IX1 can be explained as arising from
unanticipated behavior of Isi, and IX1 does not necessarily play a key role
in generating Purkinje fiber electrical activity.
