the channel to revert back to its initial resting,
closed state. Full recovery of the h-gates can
take 100 milliseconds or longer after the rest-
ing membrane potential has been restored.
The response of the activation and inac-
tivation gates described above occurs when
the resting membrane potential is normal
(about -9 0 mV) and a rapid depolarization
of the membrane occurs, as happens when a
normal depolarization current spreads from
one cardiac cell to another during electri-
cal activation of the heart. The response of
the fast sodium channel, however, is differ-
ent when the resting membrane potential
is partially depolarized or the cell is slowly
depolarized. For example, when myocytes
become hypoxic, the cells depolarize to a less
negative resting membrane potential. This
partially depolarized state inactivates sodium
channels by closing the h-gates. The more a
cell is depolarized, the greater the number of
inactivated sodium channels. At a membrane
potential of about -55 mV, virtually all fast
sodium channels are inactivated. If a myocyte
has a normal resting potential but then under-
goes slow depolarization, more time is avail-
able for the h-gates to close as the m-gates are
opening. This causes the sodium channel to
transition directly from the resting (closed)
state to the inactivated (closed) state. The
result is that there is no activated, open state
for sodium to pass through the channel, effec-
tively abolishing fast sodium currents through
these channels. As long as the partial depolar-
ized state persists, the channel will not resume
its resting, closed state. As described later in
this chapter, these changes significantly alter
myocyte action potentials by abolishing fast
sodium currents during action potentials.
A single cardiac cell has many sodium
channels, and each channel has a slightly dif-
ferent voltage activation threshold and dura-
tion of its open, activated state. The amount
of sodium (the sodium current) that passes
through sodium channels when a cardiac cell
undergoes depolarization depends upon the
number of sodium channels, the duration
of time the channels are in the open state,
and the electrochemical gradient driving the
sodium into the cell.
The open and closed states described for
sodium channels are also found in other ion
channels. For example, slow calcium chan-
nels have activation and inactivation gates
(although they have different letter designa-
tions than fast sodium channels). Although
this conceptual model is useful to help under-
stand how ions transverse the membrane,
many of the details of how this actually occurs
at the molecular level are still unknown. Nev-
ertheless, recent research is helping to show
which regions of ion channel proteins act as
voltage sensors and which regions undergo
gates described in the conceptual model.
Action Potentials
Action potentials occur when the membrane
repolarizes back to its resting state. The two
general types of cardiac action potentials
include nonpacemaker and pacemaker action
potentials. Nonpacemaker action potentials
are triggered by depolarizing currents from
adjacent cells, whereas pacemaker cells are
capable of spontaneous action potential gen-
eration. Both types of action potentials in
the heart differ considerably from the action
potentials found in nerve and skeletal muscle
cells (Fig. 2.4). One major difference is the
duration of the action potentials. In a typical
nerve, the action potential duration is about 1
Time (ms)
■ FIGURE 2.4 Comparison of action potentials
from a nerve cell and a nonpacemaker cardiac
myocyte. Cardiac action potentials are much
longer in duration than nerve cell action potentials.
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