About the role of shear stress in atherogenesis
Authors: S Bakker
Journal: Cardiovascular Research (2000)

See article by Gosnach et al. [22] ( pages 486 -492) ininflux of monocytes, and proliferation of resident macrothis issue.phages and smooth muscle cells.Together these factors represent the atherosclerotic inflammatory process.As blood flows through a vessel, it exerts a physicalIn contrast, steady laminar shear stress promotes release force on the vessel wall.This force can be resolved into of factors from endothelial cells that inhibit coagulation, two principal vectors [1].One, shear stress, is parallel to migration of leukocytes, and smooth muscle cell proliferthe vessel wall.It represents the frictional force that the ation [3].Apart from this growth inhibitory effect of steady flow of blood exerts at the endothelial surface of the vessel laminar shear stress on the vessel wall, it causes smooth wall.The other, tensile stress, is perpendicular to the vessel muscle cell relaxation and, consequently, vasodilatation.In wall.It represents the dilating force of blood pressure on animal experimental models stimulation of endothelial the vessel wall.The whole vessel wall, including the nitric oxide production has been identified to play an endothelium, smooth muscle cells and the extracellular important role in the vasodilatation that occurs within matrix, is exposed to it.In contrast, only the inner surface seconds after the application of increased shear stress of the vessel wall, the endothelial cells, are exposed to the [16][17][18].The measurement of the magnitude of endofrictional force of shear stress.There is some slow thelium-dependent vasodilatation in response to reactive transmural flow around smooth muscle cells in arterial hyperaemia, which is widely used in humans to assess walls, but this force is considered insignificant when endothelial function, is derived from this physiological compared with the tensile wall stress to which these cells phenomenon [19,20].It has been documented in many are exposed [2].animal experimental studies that vasodilatation also occurs Many lines of evidence are consistent with the view that in response to a chronic increase in shear stress.However, a chronic exposure of endothelial cells to high levels of in this setting more factors are involved than nitric oxide shear stress with little temporal fluctuations causes them to alone.It is accompanied by a shift in the balance of release exhibit an atheroprotective phenotype [3].In vivo studies of vasoactive substances and growth-promoting and inhibin humans have demonstrated that areas of the arterial wall iting factors by endothelial cells towards vasodilatation and that are exposed to low mean shear stress and oscillatory antiproliferation [3,21].flow with flow reversal are associated with localised A stimulation of angiotensin converting enzyme (ACE) endothelial cell dysfunction and atherosclerotic plaque activity in endothelial cells by shear stress, as reported by formation [3][4][5][6][7].Animal experimental studies have shown Gosnach et al. in this issue of the journal [22], seems to be that endothelial cells in these low shear stress regions are inconsistent with the above-described view.A higher ACE characterised by a rounded shape, increased proliferation activity stimulates the production of angiotensin II, a rate and increased permeability [8][9][10][11][12][13][14][15].In these parts of potent vasoconstrictive and growth-promoting agent.The arterial vessels there is an increased uptake of lipoproteins, authors argue that the in vitro finding of a higher ACE appearance of leukocyte adhesion molecules on the surface activity corresponds with observations of reduced lungof endothelial cells and leukocyte migration [3,15].Secre-tissue ACE activity in an in vivo study of experimental tion of chemotactic factors and growth factors causes congestive heart failure [23].They also argue that similar results have been reported in pulmonary hypertension [24].However, this latter study made a differentiation between