Biomedical Engineering Reference
In-Depth Information
Tabl e 5. 9.
Cardiomycyte and its main ion carriers in sarcolemma and membrane of the sarcoplas-
mic reticulum as well as ion fluxes between the cytosol and either the extracellular space or the
sarcoplasmic reticulum.
Carrier
Ion flux
(with respect to cytosol)
Sarcolemma
Ca
+
influx
Ca
V
channels
Ca
2
+
AT P a s e
C a
2
+
efflux
Na
+
-Ca
2
+
exchanger
Ca
2
+
efflux (forward mode)/influx (reverse mode)
Na
+
influx (forward mode)/efflux (reverse mode)
Na
+
influx
Na
V
channels
Na
+
-K
+
AT P a s e
N a
+
efflux
K
+
influx
K
+
channels
K
+
efflux
Sarcoplasmic reticulum
Ca
2
+
influx
Ryanodine receptor
Ca
2
+
AT P a s e
C a
2
+
efflux
Na
sarcolemna
cytosol
T−tubule
Ca
ATPase
K
ADP
ATP
H
mitochondrion
Na
VDCC
PLb
RC
SERCA
RC
−
Csq
VDCC
Ca
PMCA
Ca
Ca
SR
Ca
Na
Ca
K
NCX
Ca
Fig. 5.16
The cardiomyocyte and its main ion carriers. Voltage-dependent L-type Ca
2
+
channels
(VDCC, Ca
V
1.2) of the sarcolemma trigger ryanodine calcium channels (RC) of the sarcoplasmic
reticulum (SR), the main cellular storage source of Ca
2
+
ions. The cytosolic concentration of
calcium determines the number of actomyosin cross-bridges per time unit, hence the maximal
velocity of sarcomere shortening. At the end of systole, calcium dissociates from troponin-C and
is transported into the sarcoplasmic reticulum by the sarco(endo)plasmatic reticulum Ca
2
+
AT P a s e
pump (SERCA). Calcium efflux from the myocyte to the extracellular space also balances the
calcium amount that has entered due to the action potential. During relaxation, Ca
2
+
is exchanged
for Na
+
by the Na
+
-Ca
2
+
exchanger (NCX) and sarcolemmal calcium ATPase pump (PMCA).
The frequency-dependent control of Ca
2
+
flux is due to faster systolic calcium release from SR
and faster diastolic calcium reuptake by SR (positive lusitropy). Voltage-gated Ca
2
+
channels are
short-term regulators of intracellular Ca
2
+
level. An accumulation of cytosolic calcium increases
the force of contraction.
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