Smooth Myocytes - Tissue Functioning and Remodeling in the Circulatory and Ventilatory Systems - page 435

Table 8.22. Direct vasodilators that activate GPCRs on vascular smooth myocytes
(Source: [ 812 ]). G-protein-coupled receptors on vascular smooth myocytes are predominantly
coupled to Gs. Ligand binding to these GPCRs activates adenylate cyclase, thereby increasing
the intracellular cAMP concentration that stimulates protein kinase-A to reduce the sensitivity
of stress fibers to calcium ions and favor vasodilation. In addition, G βγ can cause membrane

hyperpolarization by K + efflux.

GPCR Type Agonist

β

1/2/3 Adrenaline

5HT 7 Serotonin

D 1 Dopamine

H 2 Histamine

A 2A / 2B Adenosine

Ghrelin receptor Ghrelin

AM Adrenomedullin

CGPR 1 Adrenomedullin, amylin, CGRP

NOP Nociceptin

CRF 2 Urocortins

V 2 Vasopressin

VPAC Vasoactive intestinal peptide

DP Prostaglandin-D2

EP 4 Prostaglandin-E2

IP 1 Prostacyclin

membrane, 5-lipoxygenase and 5LOx-activating protein can associate with integral
membrane LTc4 synthase to generate LTc4. The latter is exported by multidrug
resistance-associated protein to the extracellular medium, where it is cleaved
into LTd4 and LTe4 by extracellular peptidases. In addition to 5-lipoxygenase,
(12,15)LOx lodges in some tissue-resident macrophages, but not in circulating
monocytes.

Apelins

Apelins are potent vasoconstrictors in endothelium-denuded arteries and veins that
can mediate vasodilation via vasodilators released from endothelial cells that operate
on nearby smooth myocytes [ 812 ]. Apelin 36 localizes to endothelial cells of small
arteries.

Motilin

Vasoconstrictor motilin is able to provoke endothelium-dependent relaxation of
coronary arteries [ 812 ]. Motilin receptors on smooth myocytes can be activated by
circulating motilin or that released from nerve terminals of arteries and veins.