Biomedical Engineering Reference
In-Depth Information
Table 8.23.
Indirect vasodilators that activate GPCRs on vascular endothelial and smooth my-
ocytes (Source: [
812
]). A large number of GPCRs localize to endothelial cells. Their activation
creates an increase in the concentration of free cytosolic Ca
2
+
that can generate and release
prostacyclin, nitric oxide, or endothelium-derived hyperpolarizing factors. These agents diffuse
onto the underlying smooth myocyte to activate their cognate GPCRs, soluble guanylate cyclase,
and protein kinase-G, or produce membrane hyperpolarization (CGRP: calcitonin gene-related
peptide).
GPCR Type
Agonist
M
1
/
3
Acetylcholine
α
2a,
β
2/3
Adrenaline
H
1
Histamine
P2Y
1
ADP
P2Y
2
AT P, U T P
AMR
Adrenomedullin
CGPR
1
Adrenomedullin, CGRP
B
1
/
2
Bradykinin
ET
B
Endothelin-1
Motilin receptor
Motilin
NK
1
Substance-P
V
1
/
2
Vasopressin
VPAC
Vasoactive intestinal peptide
FP
Prostaglandin-F2
α
PAFR
Platelet-activating factor
CysLT
1
Leukotriene-D4
CysLT
2
Leukotriene-C4
S1P
1
/
3
Sphingosine 1-phosphate
PA R
1
Thrombin
PA R
2
Serine peptidases
Urotensin-2
Urotensin-2 has antagonist effects in distinct vascular networks, as it can behave
as a potent vasoconstrictor or a vasodilator. Besides, it can have no vasoactivity.
Its vasodilation effect requires a functional endothelium. In humans, resistance
coronary arteries are much more sensitive to urotensin-2 than epicardial distribution
arteries [
812
]. Urotensin-2 as well as vasodilator ghrelin reside in endothelial
cells and their receptors have been identified on vascular smooth myocytes [
812
].
Urotensin-2 is also observed in regions of infiltrating macrophages within the
atheromatous lesion.
Sphingosine 1-Phosphate
Sphingosine 1-phosphate operates as a vasoconstrictor via S1P
2
and/or S1P
3
receptors, whereas endothelium-dependent vasodilation is mediated via S1P
1
and
possibly S1P
3
receptors [
812
]. Vasoconstricting effect of S1P may be more impor-
tant in small arteries.
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