Mechanical Stress and Arterial Remodeling

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An arterial wall is a complex tissue composed of different cell populations capable of structural and functional changes, in response to direct injury and atherogenic factors, or to modifications of long-term hemodynamic conditions. The principal geometric modifications induced by hemodynamic alterations are changes of arterial lumen and/or arterial wall thickness due to activation, proliferation and migration of VSM cells, and rearrangements of cellular elements and ECM [12-18].

The mechanical signals for arterial remodeling associated with hemody-namic overload are cyclic tensile stress and shear stress [13-17]. BP is the principal determinant of arterial wall stretch and tensile stress, creating radial and tangential forces that counteract the effect of intraluminal pressure. Blood-flow alterations result in changes of shear stress, the dragging frictional force created by blood flow. While acute changes in tensile or shear stress induce transient adjustments in vasomotor tone and arterial diameter, chronic alterations of mechanical forces lead to modifications of the geometry and composition of the vessel walls [15].

According to Laplace's law, tensile stress (ct) is directly proportional to arterial transmural pressure (P) and radius (r), and inversely proportional to arterial wall thickness (h) according to the formula ct = Pr/h [1-3,14]. In response to increased BP or arterial radius, tensile stress is maintained within the physiological range by thickening of the heart and vessel walls, a process which is constantly observed in the cardiovascular (CV) system of atherosclerotic or hypertensive subjects [14-16, 18]. Due to a very low stress level, this process cannot be clearly observed or is even absent at the site of smaller arterioles or capillaries.

Shear stress is a function of the blood-flow pattern. In 'linear' segments of the vasculature, blood is displaced in layers moving at different velocities [1, 2]. The middle of the stream moves more rapidly than the side layers, generating a parabolic velocity profile. The slope of the velocity profile, i.e., the change of blood velocity per unit distance across the vessel radius, defines the shear rate. Shear stress is the product of the shear rate X blood viscosity. Thus, shear stress (t) is directly proportional to blood flow (Q) and blood viscosity and inversely proportional to the radius (r) of the vessel, according to the formula t = Q^/^r3 [2, 14, 16]. Shear stress is often presented as the major mechanical factor acting in atherosclerosis while tensile stress is rather acting in hypertension. In fact, changes in shear and tensile stress are interconnected, because any modification of the arterial radius caused by alterations in blood flow and shear stress induces changes in tensile stress (unless the BP varies in the opposite direction).

The characteristics of arterial remodeling depend largely on the nature of hemodynamic stimuli applied to the vessel. To maintain tensile stress within physiological limits, arteries respond by thickening their walls (Laplace's law), but the increased tensile stress results from both the direct effect of high BP and the pressure-dependent passive distension of the arterial lumen. Studies in animals and humans have shown that this pressure-related distension of the arterial diameter is limited to central (elastic-type) arteries, being absent from peripheral (muscular-type) arteries, and causes an increase of the wall-to-lumen ratio which is proportional to the pressure [2, 3, 14]. The limitation or absence of a pressure-dependent diameter increase efficiently maintains tensile stress within normal limits. The nature of the mechanism(s) preventing the passive 'dilatory' effect of pressure is unknown but requires the presence of an intact endothelium [14]. Pertinently, but beyond the scope of this chapter, endothelial function is consistently altered in subjects with hypertension and/ or atherosclerosis [14, 15, 19].

Experimental and clinical data indicate that acute and chronic augmentations of arterial blood flow induce proportional increases in the vessel lumen, whereas decreasing flow reduces the arterial inner diameter [14, 15]. An example of flow-mediated remodeling associates arterial dilation and sustained high blood flow after the creation of an arteriovenous fistula [20]. Increased arterial inner diameter is usually accompanied by wall hypertrophy and increased intima-media cross-sectional area (following increases in the radius and wall tension). The presence of the endothelium is a prerequisite for normal vascular adaptation to chronic changes of blood flow, and experimental data indicate that flow-mediated arterial remodeling can be limited through inhibition of NO synthase [19]. Finally, although the alterations of tensile and shear stresses are interrelated, changes of tensile stress primarily induce alterations and hypertrophy of the arterial media, whereas changes of shear stress principally modify the dimensions and structure of the intima.

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