Since the mid-1970s, we have continued to understand better the fundamental importance of mechanotransduction in vascular biology. For example, beginning with Rosen and colleagues in 1974, we discovered that endothelial cells alter their production of vasoactive molecules in response to changes in flow-induced wall shear stress; beginning with Glagov and colleagues in 1976, we discovered that vascular smooth muscle cells alter their production of extracellular matrix proteins in response to changes in cyclic stretching comparable to that induced by pulsatile pressures [1]. Indeed, such findings are not surprising given the well know arterial adaptations that occur in response to sustained changes in blood flow or pressure. The caliber of an artery tends to increase (or decrease) in response to sustained increases (decreases) in blood flow and the thickness of the arterial wall tends to increase (or decrease) in response to sustained increases (decreases) in blood pressure. In both cases, it appears that the associated wall shear or intramural circumferential stresses are returned toward normal following the change in hemodynamics.

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