Mechanisms involved in endothelial responses to hemodynamic forces

Abstract

Blood flow in arteries, arterioles and pre-capillary vessels generates hemodynamic shear stresses. These typically range from 0 to 50 dyn/cm2 and vary in magnitude, frequency and direction at the endothelial surface throughout the cardiac cycle [1]. In addition to flow-mediated vasotonic control, hemodynamic forces play a pivotal role in atherosclerotic lesion development in humans. Lesions tend to develop in areas where there is a deviation from unidirectional laminar blood flow, typically near branches, bifurcations, regions of arterial narrowing and curvature. Mechanisms responsible for the transmission and transduction of hemodynamic information from the blood to the underlying vessel wall reside in the endothelium [2]and considerable progress has been made in determining the signaling events at the cell surface(s) and the gene regulatory elements associated with cellular adaptation to mechanical stress [3, 4].