Going With the Flow

The predilection of atherosclerosis for specific locations inthe vasculature strongly suggests that the response of the arterial wall to alterations in blood flow is an important factor in vascular disease pathogenesis. Turbulent rather than lam-inar blood flow reduces shear stress and leads to endothelial cell dysfunction.1 Better understanding of the mechanisms linking laminar shear stress to endothelial cell homeostasis would improve our knowledge of the pathogenesis of athero-sclerosis and may provide new therapeutic targets to combat vascular disease. One major effect of laminar shear stress on endothelial cells is the increased production of nitric oxide (NO), through increased expression of endothelial nitric oxide synthase (eNOS) and by eNOS activation through phosphorylation.2 However, upregulation of eNOS protein alone can have paradoxical deleterious effects on vascular disease pathogen