Vascular Endothelium - Tissue Functioning and Remodeling in the Circulatory and Ventilatory Systems - page 491

KCa

+

−

K

ECM

hyperpolarization

K pool K

TREK1

EC

myoendothelial gap junction

SMC

hyperpolarization
spreading

K

cell membrane
polarization
change

Kir

K

Na−−K−ATPase

vasodilation

Fig. 9.4 Potassium channels in vascular endothelial cells and smooth myocytes cooperate to
regulate the vasomotor tone either via the extracellular matrix (ECM) or myoendothelial junctions.

vascular endothelial cells and smooth myocytes participates in the paracrine control
of smooth myocytes by endothelial cells; TGF

β

that acts on endothelial cells, but
not on smooth myocytes, is implicated in the feedback from smooth myocytes to
endothelial cells.

9.5.5.1 Acetylcholine

Acetylcholine is synthesized and stored by choline acetyltransferase in endothelial
cells of small brain vessels [ 901 ] and rat coronary arteries [ 904 ]. Acetylcholine is
an NOS3 activator.
In coronary arteries, acetylcholine effect varies according to its concentration
and the context (apparently normal or observed atheroma). In normal coronary
arteries, vasodilation mediated by NO released from endothelial cells subjected
to low acetylcholine concentrations via endothelial muscarinic M 3 receptors, 49
whereas vasoconstriction mediated by a direct action on smooth myocytes via their

49 Muscarinic M 2 receptors localize mainly in the acrdiac atria, whereas M 3 receptors reside in
vascular smooth muscle and endothelial cells. Muscarinic M 3 receptor is coupled to Gq subunit and
phospholipase-C. The latter splits plasmalemmal phosphatidylinositol (4,5)-bisphosphate (PIP 2 )
into inositol trisphosphate and diacylglycerol. The former targets IP 3 receptors that release Ca 2 +
from the endoplamic reticulum. In smooth myocytes, Ca 2 + primes contration. In endothelial cells,
Ca 2 + activates nitric oxide synthase.