Short-Term Biomechanical Adaptation of the Rat Carotid to Acute Hypertension: Contribution of Smooth Muscle

Abstract

The biomechanical adaptation of the arterial wall to hypertension has been studied extensively in recent years; however, the exact biomechanical contribution of vascular smooth muscle cells (VSMCs) during the adaptation process in conduit vessels is not known. We induced hypertension in 8 wk old Wistar rats by total ligation of the aorta between the two kidneys. Mean blood pressure increased from 92 +/- 2 (mean +/- SE) mm Hg to approximately 150 mmHg. Rats were sacrificed 2, 4, and 8 d after surgery and the left common carotid artery was excised for analysis. Wall thickness increased by 18% in 8 d and the opening angle by 32% in 4 d. The elastic properties were measured under normal VSMC tone (i.e., the amount of VSMC tone under normal conditions also called basal VSMC tone or normal resting VSMC tone), under maximally contracted VSMC (NE, 5 x 10(-7) mol/L) and under totally relaxed VSMC conditions (papaverine, 10(-4) mol/L). The most pronounced modifications were the changes in elastic properties related to normal VSMC tone. The functional contraction ratio at 100 mm Hg, defined as the relative contraction under normal conditions (normal VSMC tone), increased by 439% 4 d after the induction of hypertension. The total contraction capacity of the VSMC increased by 38% within 8 d. The changes in normal VSMC tone led to important changes in the mechanical properties of the arterial wall. Under normal VSMC conditions, compliance at mean pressure (148 mm Hg) increased by 159% within 8 d, whereas in the absence of VSMC tone, compliance did not increase significantly. We conclude that in conduit vessels, the VSMC, which is the sensing and effecting element of the adaptation process, is subjected to large-scale changes during the early phase of arterial adaptation to acute hypertension.

Biomechanical response of femoral vein to chronic elevation of blood pressure in rabbits

“…For example, Matsumoto and Hayashi (26,27) have demonstrated in the rat with induced Goldblatt hypertension that the aortic hoop stress at in vivo pressure was rapidly returned to a physiologically normal level, i.e., within 2 wk after the induction of hypertension and remained at the level, thereafter, and that the elastic modulus of wall at the in vivo pressure became a normal value after a relatively long period of time, i.e., at 16 wk after the induction of hypertension. In addition, Fridez et al (8,9) have shown in a rat model with abdominal aortic ligation that the vascular smooth muscle cell, which is the sensing and effecting element of the adaptation process, is activated during the early phase of arterial adaptation to hypertension. Furthermore, there are many studies showing that arteries change the internal diameter in response to blood flow change keeping wall shear stress at normal, constant levels if the flow change is within a certain range (for example see Refs.…”

“…It has also been shown that vascular smooth muscle cells (8,21,37) and endothelial cells (22,49) play important roles in the control of wall hoop stress and wall shear stress, respectively. On one hand, there are many studies on the response of in vitro cultured cells to stress, which have indicated that stress affects the proliferation and function of vascular smooth muscle cells (46,48) and endothelial cells (14,45,47).…”

“…On one hand, the elastic modulus of the wall, which was also high soon after the induction of hypertension, became normal after a relatively long period of time, i.e., at 16 wk. In addition, Fridez et al (8,9) have shown that normal vascular tone related to the smooth muscle cell, which is the sensing and effecting element of the adaptation process, was increased during the early phase of arterial adaptation to hypertension.…”

Twin-Twin Transfusion Syndrome

“…A rapid increase in intravascular pressure in animals (equivalent to the recipient twin) results in vascular smooth muscle contraction and increased resistance and medial thickness. Over a month, as the smooth muscle tone returns to normal, this increased medial thickness is maintained by remodeling 23 to preserve a constant wall stress. These changes imply that the recipient twin exposed to an acute transfusional load should have increased PWV (as seen in 1 recipient of the 3, with an acute intertransfusional process in group 1).…”

Early Changes in Vascular Dynamics in Relation to Twin-Twin Transfusion Syndrome

“…The vascular response to hypertension in the adult human is that of an increase in the diameter of the artery, reduced compliance and an increase in pulse pressure to reduce wall stress. Evidence from animal studies suggests that the immediate response to a rapid increase in intravascular pressure is dominated by a change in vascular smooth muscle contractile state and that over a period of a week this increased resistance is maintained by remodelling (Fridez et al, 2001). These adaptive changes remain when blood pressure is reduced experimentally in animal experiments.…”