Tissue Development, Repair, and Remodeling - Tissue Functioning and Remodeling in the Circulatory and Ventilatory Systems - page 738

communications in skeletal muscle resistance arteries [ 1488 ]. Wall distensibility is
more progressively restored. The mechanical changes occur during the second stage
of wall remodeling.
Under sustained hypertension, the wall thickness of segments of the descending
thoracic aorta increases in hypertensive dogs with respect to normotensive dogs,
with a concurrent prestress reduction and an axial stiffening increase [ 1489 ].
Wall thickness of rat thoracic aortas correlates significantly with systolic blood
pressure [ 1490 ]. The wall elastic moduli of hypertensive rats becomes equal to the
normal values after a relatively long time.
Rapid changes in stiffness of the basilar artery occurs during hypertension, with
increased collagen content in the media and adventitia and in smooth myocytes
in the media, within 2 weeks after the initiation of hypertension, using an aortic
coarctation model [ 1491 ].
Hypoxia-induced pulmonary hypertension leads to remodeling of pulmonary
vessels and right ventricular hypertrophy. Pulmonary vessel remodeling is char-
acterized by wall thickening, collagen deposition, and infiltration by pulmonary
macrophages.
Vascular smooth myocytes participate, in response to hypertension, in
geometrical and rheological adaptation, characterized not only by SMC proliferation
but also migration, with myogenic adjustment. Vascular smooth myocytes migrate
from the media into the intima, proliferate, synthesize extracellular matrix, and
form the neointima. Hypertension induces change in vasomotor tone and wall
circumferential stress [ 1492 ].
Flow-dependent remodeling is more pronounced in muscular arteries than in
elastic arteries. These regional differences may be associated with the local flow
pattern and the quantity of smooth myocytes and matrix components.
The arterial wall layers non-uniformly thicken during induced hypertension
[ 1493 ]. The inner wall layers thicken more in the acute phase of hypertension,
whereas the outer layers are thicker than the inner strata when the vessel is subjected
to long-term (up to 56 days) hypertension. The medial collagen content quickly
increases during the acute hypertension phase and slowly later. The elastin level
slightly and steadily increases. Vascular smooth muscle tone rapidly rises and nearly
returns to control levels.
Hypertensive remodeling is characterized by wall accumulation of collagen-1, -
3, and -4 to counteract wall distention, but it yields wall stiffness. However, released
matrix metallopeptidases, especially MMP9 [ 1494 ], lead to wall degradation with
subsequent enhanced wall distensibility.
Nitric oxide is a predominant mediator of vasodilation and remodeling in
response to increased wall shear stresses. NO release from endothelial cells exposed
to excessive shear triggers a set of events, including growth factor induction
and MMP activation, which together contribute to restructuring of the vessel
wall [ 1495 ]. Moreover, degradation by MMP can overcome concomitant matrix
synthesis. Although the elastic content remains normal, fragmentations in medial
elastic laminae induce vessel tortuosity.