Smooth Myocytes - Tissue Functioning and Remodeling in the Circulatory and Ventilatory Systems - page 403

Vascular smooth myocytes are responsible for vasomotor tone using

actin-myosin filaments. The contractile apparatus of differentiated smooth

myocytes encompasses smooth muscle isoforms of α -actin, myosin heavy chain,

calponin-1, 28 transgelin-1, and smoothelin.
The vasomotor tone depends on sympathetic innervation and neurohumoral
vasoactive command as well as various types of mechanotransduction processes
according to the region within the arterial compartment (large arteries to minimize
cardiac postload, small arteries and arterioles to maintain a constant nutritive blood
flow, and small arterioles to fit the local metabolism needs).
Arterial smooth myocytes regulate blood pressure and flow according to cardiac
postload and tissue metabolism needs. In the microvasculature, smooth muscles
construct precapillary sphincters that regulate blood flow in capillary beds.
Vascular smooth myocytes include phasic and tonic varieties. The tonic type does
not generate action potentials, whereas the phasic type in the portal system and
lymphatics creates contraction waves to propel luminal fluid toward the heart.
Vascular smooth myocytes also differ according to vascular compartment
(whether they pertain to an artery or a vein, to a large artery or resistance arteriole),
embryological origin, and organ-dependent microenvironment.
Due to blood pressure-dependent radial hydraulic conductance, the arterial
circulating plasma molecules are outwardly convected. Transferred macromolecules
within the vessel wall act as extrinsic stimuli of mural cells. Vascular smooth
myocytes can reprogram their expression pattern in response to acute and chronic
stimuli. In addition, mechanical signals can directly (blood pressure-derived intra-
mural tension) or indirectly (shear rate-induced endothelial command) influence the
vSMC phenotype. In particular, arterial smooth myocytes respond to hypertension
and resulting increase in wall tension by hypertrophy and secreting extracellular
matrix constituents via RhoA, ERK1, and ERK2 [ 745 ].
Differentiated vascular smooth myocytes are also able to modify their phenotype
in response to vessel wall inflammation or injury. In healthy vasculature, smooth
myocytes remain quiescent and highly contractile; in disorders of the arterial wall,
smooth myocytes adopt a proliferative phenotype and loose their non-contractile
phenotype. Vascular diseases (aneurysm, atherosclerosis, hypertension, and post-
stenting restenosis; Vol. 6 - Chap. 8. Vascular Diseases) are generally characterized
by smooth myocyte phenotype switching. In response to vessel damage, smooth
myocytes dedifferentiate and cause intimal hyperplasia. They proliferate, migrate

28 Calponins that abound in smooth myocytes are encoded by 3 genes. The most abundant form
is calponin-1, also called α -calponin, basic calponin, and H1-calponin (292 amino acids, i.e., a
long form [calponin-1 S ]), which is encoded by the CNN1 gene. β -Calponin that is also encoded
by the CNN1 gene represents a short isoform (252 amino acids; calponin-1 S ). Two other genes
encode calponin-2 (neutral calponin or H2-calponin), and calponin-3 (acidic calponin), which are
expressed at lower levels in smooth and non-muscle cells. Other members of the calponin family
that are more widely synthesized include transgelin-1, or SM22

α β

, and transgelin-2, or SM22 ,

encoded by the TAGLN and TAGLN2 genes.