Biomedical Engineering Reference
In-Depth Information
Table 8.10.
Calcium transport in myocytes. Phosphorylation by cAMP-dependent protein kinase
acts for channel opening. PKA also phosphorylates phospholamban to increase SERCA activity.
Transport path
Activity
Influence factor
Sarcolemma
Ca
2
+
influx
Voltage-dependent
PKC
channel
Ca
V
1
Slow inactivation
PKA
Ca
V
3
Quick inactivation
Ca
2
+
influx
Strech-activated
channel
Ca
2
+
influx
Receptor-operated
α
1
-Adrenergic receptor
channel
Ca
2
+
efflux
ATPase pump
Cam
Na
+
-Ca
2
+
exchanger
Ca
2
+
efflux
Endo(sarco)plasmic reticulum
Ca
2
+
influx
Ryanodine-sensitive
Ca
2
+
-sensitive
Ca
2
+
influx
Ca
2
+
influx
IP
3
-sensitive
channel
SERCA
Ca
2
+
resequestration
PLb
Mitochondrion
Ca
2
+
uniporter
Ca
2
+
uptake
into distinct bands, but organized for maintainance of tonic contractions. Vascular
smooth muscle contraction can be initiated by mechanical, electrical, and chemi-
cal
41
stimuli, in particular SMC stretching causes contraction (myogenic response).
Manifold isoforms of actin [
758
] and myosin light and heavy chains [
759
]exist.
The difference in isoforms of contractile proteins between small and large arteries
may induce different characteristics. SMC contraction speed is very low, but can
achieve a much greater degree of shortening.
Activity of smooth myocytes is regulated by cytosolic calcium concentration
i
) due to: (1) membrane depolarization and Ca
2
+
entry from the extracellular
medium via plasmalemmal, voltage-gated Ca
V
1andCa
V
3 channels (Fig.
8.1
);
(2) Ca
2
+
release through ryanodine receptors from endoplasmic reticulum; and
(3) receptor-dependent Ca
2
+
channels (Table
8.10
).
Ca
2
+
]
[
(
41
Noradrenaline,
angiotensin-2, vasopressin,
endothelin-1, and thromboxane-A2
cause SMC
contraction.
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