Flow, NO, and atherogenesis - PubMed (original) (raw)

Figure 1

Vascular effects of laminar or disturbed flow. The tractive force of fluid flow, i.e., shear stress, is sensed by the endothelium; the signal transduction apparatus is incompletely characterized but involves activation of specific kinases and ion channels that induce the release of vasoactive factors and the expression of genes affecting vascular function and structure. The response to physiological laminar flow and disturbed flow (such as that observed at bends, branches, and bifurcations) is quite different. The response activated by disturbed flow predisposes to atherogenesis. KCa, calcium-activated potassium channel; BK, bradykinin; Ach, acetylcholine; PGI2, prostacyclin; EDHF, endothelium-dependent hyperpolarizing factor; SOD, superoxide dismutase; COX, cyclooxygenase; CAM, cell adhesion molecule (e.g., vascular cell adhesion molecule); tPA, tissue plasminogen activator; VSM, vascular smooth muscle; TGFβ, transforming growth factor β; PDGF, platelet-derived growth factor; SMAD, family of flow-regulated transcriptional factors; ET-1, endothelin; EC, endothelial cell; NFκB, Elk-1, and p-CREB, redox-activated transcriptional proteins.