In addition to the changes in functional arteriolar control mechanisms in hypertension, structural alterations of arteri-oles and small arteries can contribute to the elevated vascular resistance in this disease. These changes include structural narrowing of the lumen, thickening of the vascular wall leading to an increased wall/lumen ratio, and altered mechanical properties of the vessel, such as increased stiffness and reduced distensibility of the vessel wall. These structural alterations of the vascular wall may be caused, at least in part, by alterations in the composition of the wall, such as changes in collagen and elastin content in the vessel wall, or by alterations in the specific types of collagen present in the vascular wall.
Most reports indicate that wall thickening is not a common response to elevated blood pressure in the smaller arte-rioles; however, wall thickening is prominent in the larger arteries that lie upstream from the microcirculation. There is evidence that the nature of the structural alterations occurring in the vascular wall in response to hypertension may be determined by the response of individual vessels to the increase in circumferential wall stress occurring during elevations in arterial pressure. In large arteries or in resistance arteries that do not exhibit strong myogenic responses, hypertrophy of the smooth muscle cells and the deposition of extracellular matrix thicken the walls of the vessel during the development of hypertension without reducing the size of the lumen. In contrast, small arteries and arterioles that exhibit myogenic contractile activation in response to elevated pressure show an inward remodeling that reduces lumen diameter without thickening the vessel wall. This inward remodeling is mediated through the rearrangement of the smooth muscle cells around a smaller lumen. In this case, the initial increase in circumferential wall stress that occurs in response to increased pressure in the vessel can account for inward remodeling because myogenically active small arteries and arterioles can constrict in response to an elevation of intravascular pressure, thus restoring circumferential wall stress toward control levels. In contrast, larger arteries have little or no myogenic response and respond to the increase in wall stress by initiating growth processes in the vascular wall. There is substantial evidence that the structural alterations in small arteries of hypertensive individuals reflect an adaptation to the elevated blood pressure, rather than being the primary cause of increased vascular resistance in hypertension. However, structural narrowing of the vessel lumen and thickening of the vascular wall may play a crucial role in the maintenance and exacerbation of the elevated vascular resistance in hypertension. In this respect, elevations in vascular resistance that arise from structural alterations are less responsive to therapeutic approaches than those that result from an elevated vascular smooth muscle tone, which can be treated with drugs that lead to vascular smooth muscle relaxation.
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Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...