Biomedical Engineering Reference
In-Depth Information
Tabl e 9. 2.
Ion carriers of the myoendothelial microdomain between an endothelial cell (EC) and
adjoining smooth myocyte (SMC; source: [
858
]). Signaling in the myoendothelial microdomain
through gap junctions and calcium-activated potassium channel enables endothelium-dependent
vasodilation. Three types of nanodomains on myoendothelial microdomains (myoendothelial
projections) can be defined: (1) myoendothelial gap junction that facilitates ion transfer; (2) K
Ca
channel residence; and (3) transient receptor potential (TRP) channel (non-selective cation carrier)
site (TRPC3: type-3 TRP canonical; TRPV4: type-4 TRP vanilloid). The 2 latter nanodomains can
merge.
Gap junction (myoendothelial feedback)
Molecular transfer
Ions, IP
3
Endothelial projection membrane
K
+
export (from EC cytosol)
K
Ca
3.1 (IK)
Ca
2
+
import (into EC cytosol)
TRPC3
Ca
2
+
import
TRPV4
Endothelial projection endoplasmic reticulum membrane
IP
3
R
Ca
2
+
release
Smooth myocyte membrane
Na
+
-K
+
AT P a s e
K
+
entry (into SMC cytosol)
Na
+
efflux (from SMC cytosol)
K
+
influx
K
IR
Tabl e 9. 3.
Features
of
myoendothelial
microdomains
in
human
mesenteric
arteries
(Source: [
857
]; MEGJ: myoendothelial gap junction).
Number of SMC layers
∼
7
Adventitial thickness
10.8
±
1.1
m
1.9
±
0.7
×
10
3
m
2
MEGJ density
10
3
m
2
K
Ca
3.1
4.1
±
0.6
×
10
3
m
2
Connexin-37
2.2
±
0.5
×
K
Ca
3.1) that mainly localize to the myoendothelial projections. The contribution of
SK
Ca
and IK
Ca
channels varies between species as well as in different vascular beds
of the same species [
857
].
The opening of endothelial Ca
2
+
-sensitive K
Ca
3.1 channels on myoendothelial
projections elevates the extracellular K
+
concentration in the myoendothelial space
that activates inwardly rectifying K
+
channels, which may lodge exclusively on
the endothelial surface (in rat mesenteric artery), and Na
+
-K
+
pumps on smooth
myocytes adjacent to myoendothelial projections, at least in small resistive arteries,
thereby hyperpolarizing these cells [
859
].
In fact, endothelium-dependent vasodilation, at least in human mesenteric
arteries, is primarily mediated by [
857
]: (1) nitric oxide; (2) NO- and PGi2-
independent endothelium-derived hyperpolarizing current through IK
Ca
channel;
and (3) NO- and PGi2-independent material transfer through gap junction connexin-
37 (Table
9.3
).
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