8/12/2019 The First Phase of the Cardiac Contractile Action
Potential is the Rapid Depolarization Phase
1/2
The first phase of the cardiac contractile action potential is
the rapid depolarization phase. This
phase involves the opening of the fast Na+channelscausing a
rapid increase in the membrane
conductance to Na+and thus a rapid influx of Na
+ions into the cell. The ability of the cell to
open the fast Na+channels during the rapid depolarization phase
is related to the membrane
potential at the moment of excitation. If the membrane potential
is at its baseline (about -85 mV),
all the fast Na
+
channels are closed, and excitation will open them all, causing
a large influx ofNa+ions. If, however, the membrane potential is
less negative, some of the fast Na
+channels
will be in an inactivated state insensitive to opening, thus
causing a lesser response to excitation
of the cell membrane and a lower Vmax. For this reason, if the
resting membrane potential
becomes too positive, the cell may not be excitable, and
conduction through the heart may bedelayed, increasing the risk
forarrhythmias.
The fastsodium channelcan be modeled as being controlled by a
number ofgates. Each gate (orgating variable) can attain a value
between 1 (fully open) and 0 (fully closed). The product of all
the gates denotes the percentage of channels available to
conductNa+.Following the model of
Hodgkin and Huxley,the sodium channel contains three gates: m,
h, andj. In the resting state,
the mgate is closed (zero) and the handjgates are open (one).
Hence, the product denoting thepercentage of conducting channels is
also zero. Upon electrical stimulation of the cell, the mgate
opens quickly while simultaneously the handjgates close more
slowly. For a brief period oftime, all gates are open
(i.e.non-zero) and Na
+can enter the cell following itselectrochemical
gradient.If, as above, the resting membrane potential is too
positive, the horjgates may be
considerably less than one, such that the product of m,
handjbecomes too small upon
depolarization.
Phase 1of the action potential occurs with the inactivation of
the fastNa+channels.The
transient net outward current causing the small downward
deflection of the action potential is
due to the movement of K+and Cl
-ions, carried by theIto1and Ito2currents, respectively.
Particularly the Ito1contributes to the "notch" of some
ventricular cardiomyocyte actionpotentials.
It has been suggested that Cl-ions movement across the cell
membrane during Phase I is as a
result of the change in membrane potential, from K+efflux, and
is not a contributory factor to the
initial repolarization ("notch").
[edit]Phase 2
This "plateau" phase of the cardiac action potential is
sustained by a balance between inward
movement of Ca2+
(ICa) through L-typecalcium channelsand outward movement of
K+through
the slow delayed rectifierpotassium
channels,IKs.Thesodium-calcium exchangercurrent, INa,Caand
thesodium/potassium pumpcurrent, INa,Kalso play minor roles during
phase 2.
[edit]Phase 3
During phase 3 (the "rapid repolarization" phase) of the action
potential, the L-typeCa2+
channelsclose, while theslow delayed rectifier(IKs)K+channelsare
still open. This ensures a
net outward current, corresponding to negative change inmembrane
potential,thus allowing
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