Biomedical Engineering Reference
In-Depth Information
Table 6.17.
Phases of action potential and main ionic motions.
Phase
Ion motion
Path
Na
+
influx
Na
+
channels (quick and short opening)
0
K
+
efflux
Transient outward K
+
channels
1
Ca
2
+
influx
2
Ca
V
1 channel, RyR
K
+
efflux
Delayed rectifier K
+
channels
3
K
+
efflux
Inwardly rectifying K
+
channels
4
6.5.2
Ventricular Action Potential
The action potential is initiated by depolarization of the sarcolemma, disturbing
the ionic gradient across the sarcolemma. Separate voltage-sensitive channels
62
for
Na
+
,K
+
,andCa
2
+
exist in the sarcolemma that transiently open and increase the
passage of these ions.
Sodium channels open first and then rapidly inactivate (Phase
0
;Table
6.17
).
The depolarization, indeed, inactivates these Na
+
channels. The quick cellward Na
+
motion increases transmembrane potential up to about
30 mV. The conductance of
the inward K
+
rectifiers strongly decreases from the onset of depolarization.
Phase
1
occurs after action potential peak. It corresponds to the first stage of
rapid repolarization associated with a transient outward motion of K
+
. Sarcolemmal
repolarization, especially the phase-1 rate that influences the number of activated
Ca
V
1 channels and ion flux rate through them, modulates the recruitment of
ryanodine channels to Ca
V
1 channels, hence Ca
2
+
flux to the sarcomere. A second
transient flux for repolarization is induced by Ca
2
+
-activated Cl
−
channels.
Phase
2
is associated with a slow inward Ca
2
+
current (
i
Ca
)forseveral
hundred milliseconds (plateau). Channel Ca
V
1 is indeed secondarily activated with
2 opening modes: mode 1 with short opening bursts and mode 2 with long-duration
opening. Calcium channels inactivate more slowly than Na
+
channels. Mode 2
Ca
2
+
channels are involved during phase 2 of action potential with Ca
2
+
flux
from extracellular space to sarcoplasm. They elicit additional Ca
2
+
release from
the sarcoplasmic reticulum for contraction with slow inactivation.
The plateau of ventricular action potentials is prolonged because K
+
currents
occur slowly and corresponding channels have a reduced conductance at positive
transmembrane potentials. K
+
effluxes from rapid (K
V
11) and slow (K
V
7) delayed
K
+
rectifiers balance the Ca
2
+
import.
The kinetics and conductance of Ca
V
1 channels and delayed K
+
rectifiers
determine plateau duration. A long action potential ensures adequate time for entry
+
62
Channel protein conformations are influenced by the membrane potential, so that voltage-gated
ion channels are only permeable over a narrow range of membrane potentials. On the other hand,
ligand-gated ion channels require specific chemical activators.
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