Affiliations: Department of Physiology, University of Arizona, Tucson, AZ, USA | Department of Physiology, Freie Universität Berlin, Arnimallee 22, Berlin, Germany
Note: [] Address for correspondence: Dr. T.W. Secomb, Department of Physiology, University of Arizona, Tucson, AZ 85724‐5051, USA. Tel.: +1 520 626 4513; Fax: +1 520 626 3376; E‐mail: [email protected].
Abstract: Responses of vascular endothelial cells to mechanical shear stresses resulting from blood flow are involved in regulation of blood flow, in structural adaptation of vessels, and in vascular disease. Interior surfaces of blood vessels are lined with a layer of bound or adsorbed macromolecules, known as the endothelial surface layer (ESL). In vivo investigations have shown that this layer has a width of order 1 μm, that it substantially impedes plasma flow, and that it excludes flowing red blood cells. Here, the effect of the ESL on transmission of shear stress to endothelial cells is examined using a theoretical model. The layer is assumed to consist of a matrix of molecular chains extending from the surface, held in tension by a slight increase in colloid osmotic pressure relative to that in free‐flowing plasma. It is shown that, under physiological conditions, shear stress is transmitted to the endothelial surface almost entirely by the matrix, and fluid shear stresses on endothelial cell membranes are very small. Rapid fluctuations in shear stress are strongly attenuated by the layer. The ESL may therefore play an important role in sensing of shear stress by endothelial cells.
