Biomedical Engineering Reference
In-Depth Information
P2X receptors,
44
and probably Na
+
-Ca
2
+
exchangers, provide alternative routes
for Ca
2
+
entry in endothelial cell. Voltage-gated Ca
2
+
channel is a potential
candidate for a sustained Ca
2
+
influx. Stretch-sensitive Ca
2
+
channel is inhibited
by PKG kinase. Calcium pumps PMCA and SERCA are responsible for efflux and
intracellular sequestration.
9.5.4.2
Calcium-Gated Potassium Channels
Certain autacoids that are released in response to chemical or mechanical stimuli
prime the endothelium-derived hyperpolarizing mechanism that contributes to
endothelial control of vascular caliber, particularly in small resistive arteries. This
process not only raises the vascular lumen, but also spread the electrochemical
signal to coordinate cell behavior along the vessel length (Sect.
9.10
).
Potassium influx can hyperpolarize the membrane potential in endothelial cells
or smooth myocytes that are coupled via myoendothelial gap junctions. Elec-
trochemical signals that originate from a cell type spread in the blood vessel
wall in all directions via gap junctions. Calcium-activated, large-conductance K
+
(BK) channels hyperpolarize vascular smooth myocytes, thus decreasing vascu-
lar tone. Calcium-activated small- (SK) and intermediate-conductance (IK) K
+
channels control NO synthesis in vascular endothelial cells. Furthermore, they
cause depolymerization of cortical actin cytoskeleton. On the other hand, activated
epithelial sodium channels (ENaC) depolarize the membrane potential and provoke
polymerization of
G
actin monomers in the cell cortex.
Endothelium-derived hyperpolarization mediates vasodilation in the skeletal
microcirculation generated by acetylcholine. Acetylcholine can then test the
respective contribution of endothelial Ca
2
+
-dependent channels K
Ca
3.1 (IK) and
K
Ca
2.3 (SK) in smooth myocyte relaxation by endothelium-derived hyperpolar-
ization in arterioles [
898
]. Channel IK is mainly involved in endothelium-derived
hyperpolarization, as blockade of SK channel does not have significant effect,
although it participates in vasodilation in the absence of IK channel. Moreover,
K
Ca
3.1 can not only initiate a response, but also contribute to signal propagation,
although it is not mandatory.
the superfamily of voltage-gated ion channels. CNGC ligand sensitivity and selectivity, ion
permeation, and gating are determined by the subunit composition of the channel complex. CNGC
activity is modulated by Ca
2
+
-calmodulin and phosphorylation. Channel CNGC1 is found in
arteries. Nitric oxide-induced cGMP can activate CNGC2 that exerts a negative feedback on Ca
2
+
entry.
44
Nucleotide (purinergic) ATP-gated receptor-channels (P2X family) are involved in mechanical
stress-induced Ca
2
+
influx.
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