Biomedical Engineering Reference
In-Depth Information
Table 8.11.
Ion channels and vasomotor tone with influence factors for involved channels
(Sources: [
768
-
771
]).
Channel
Effect
Influence factors
K
+
channels
Inward rectifier (K
IR
)
No significant role
ATP-sensitive (K
AT P
)
No significant role
Voltage-dependent (K
V
)
Repolarization
PKC
Ca
2
+
-activated (K
Ca
)
Repolarization
20 HETE (
)
Cl
−
channels
Selective (Cl
−
efflux)
No significant role
Ca
2
+
-activated
No effect
Volume-gated
No effect
Stretch-activated channels (SAC)
Non-selective cation channels (Na
+
,K
+
,Ca
2
+
)
Protein Tyr kinases are implicated in vascular smooth muscle contraction, both
upon Ca
2
+
influx and sensitization. Calcium sensitization corresponds to increased
myosin light chain phosphorylation, and hence cell contraction. Kinase RoCK is
activated by binding to RhoA
GTP
.Ca
2
+
Sensitization and the Rho-RoCK pathway
contribute to contraction of smooth myocytes in pulmonary artery in response to
acute or chronic hypoxia as well as agonist-mediated Ca
2
+
sensitization. Kinases of
the SRC family are activated by myristoylation and/or palmitoylation, translocation
to the plasma membrane, and subsequent autophosphorylation. Members of the
SRC family, such as Fyn, Src, and Yes, are activated by PGf2
in rat small
distal pulmonary artery [
772
]. They can regulate Rho activation via RhoGEF
phosphorylation. Kinases Fyn and Src have opposing effects on the formation of
intercellular junctions and focal contacts [
773
]. Kinase Fyn contributes to Ca
2
+
sensitization and stress fiber formation in smooth muscle contraction in coronary
artery mediated by sphingosylphosphorylcholine-RoCK signaling.
Protein
α
that mediates SMC relaxation binds directly to
the myosin-binding subunit (MBS) of MLC phosphatase. Disruption of the
PKG1-MBS complex prevents NO-cGMP action from myosin phosphatase
activation [
774
]. Phosphorylation of 20-kDa myosin regulatory light chain (MLC20;
a.k.a. smooth muscle isoform of myosin regulatory light chain MyLC2B and
MRLC2) triggers actin-myosin cross-bridges and actin polymerization in arterial
smooth myocytes [
775
].
kinase
PKG1
α
8.5.5.2
Production and Liberation of Peptidases
Vascular smooth myocytes produce
tissue inhibitors of metallopeptidases
and
several types of
serpins
, such as serpin-E1, or plasminogen activator inhibitor-
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