Biomedical Engineering Reference
In-Depth Information
Tabl e 5. 5.
Cardiac calcium-dependent ion fluxes upon increased cytosolic Ca
2
+
concentration
(Source: [
391
]; APD: action potential duration;
⊕
:Ca
2
+
increases conductance of ion carrier;
: inhibition). Stronger Ca
2
+
transients generate longer and briefer action potentials when ionic
currents are inward and outward, respectively. Because cardiomyocytes contain several types of
calcium-activated or -modulated ion carriers, the net effect depend on the balance between these
carriers.
Inward flux
Outward current and
reduced inward flux
(prolonged APD)
(shortened APD)
Na
+
-Ca
2
+
exchanger (
⊕
)
Ca
V
channel (
)
Non-selective Ca
2
+
-gated
Slow delayed rectifier K
+
channel (
⊕
)
a
2
+
-activated Cl
−
channel (
monovalent cation channel (
⊕
)
)
Small-conductance Ca
2
+
-activated
K
+
channel (
⊕
⊕
)
5.5
Calcium Signals
Cardiomyocyte growth and contractility are spatially and temporally regulated by a
set of ion channels, pumps, and exchangers responsible for Ca
2
+
shuttling between
the cytosol, intracellular stores, and extracellular milieu.
5.5.1
Calcium-Dependent Ion Carriers
Calcium ion inactivates voltage-dependent calcium channel, but activates other ion
carrier types. Calcium-activated ion channels in the heart include [
391
]: (1) calcium-
dependent chloride channels, which can contribute to the initial repolarization;
(2) calcium-activated non-selective monovalent cation channels, which carry in-
ward current at negative potentials; and (3) small-conductance calcium-activated
potassium channels (Table
5.5
). Whereas the rapid delayed rectifier K
+
current
(
i
K
,
r
), which is involved in repolarization phase 3, may be purely voltage dependent,
the slow delayed rectifier K
+
current
i
K
,
s
is more efficient at high cytosolic Ca
2
+
concentration [
391
].
The cardiac action potential triggers opening of Ca
V
1.2 channels. Resulting Ca
2
+
entry subsequently causes Ca
2
+
release from the endoplasmic reticulum through
ryanodine receptors. Calcium ions are removed from the cytosol, particularly by
endoplasmic reticulum uptake via sarco(endo)plasmic reticulum Ca
2
+
AT P a s e s
(SERCA) and extrusion through the plasma membrane via Na
+
-Ca
2
+
exchangers.
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