Endothelial cells are subjected to shear forces which influence import
ant cell functions. Shear stress induces cell elongation and formation
of stress fibers, increases permeability, pinocytosis and lipoprotein
internalization, is involved in the formation of atherosclerotic lesi
ons, increases the production of tissue plasminogen activator, and enh
ances von Willebrand factor release and hence platelet aggregation. It
decreases adherence of erythrocytes and leukocytes, and increases the
release of prostacyclin, endothelium derived relaxing factor, histami
ne and other compounds, but decreases erythropoietin secretion. The me
chanism of signal transduction to the endothelial cell is not known ex
actly; shear-sensitive ion channels seem to be involved. It is conclud
ed that a better understanding of shear-dependent endothelial function
s will influence pathophysiologic concepts and therapeutic interventio
ns.