Endothelial activation
[4] Elevating shear stress induces a vascular response by triggering nitric oxide synthesis and mechanotransduction pathways of endothelial cells.[5] The synthesis of nitric oxide facilitate shear stress mediated dilation in blood vessels and maintains a homeostatic status.[7] Shear stress causes endothelial cell deformation which activates transmembrane ion channels[8] Elevated wall shear stress caused by exercise is understood to promote mitochondrial biogenesis in the vascular endothelium indicating the benefits regular exercise may have on vascular function.[9] Alignment is recognized as an important mechanism and determinant of shear-stress induced vascular response; in vivo testing of endothelial cells has demonstrated that their mechanotransductive response is direction dependent as endothelial nitric oxide synthesis is preferentially activated under parallel flow while perpendicular flows activates inflammatory pathways like reactive oxygen species production and nuclear factor-κB.[12] High, uniform laminar shear stress is known to promote a quiescent endothelial cell state, provide anti-thrombotic effects, prevent proliferation, and decrease inflammation and apoptosis.