Effect of cell shrinkage on permeability of cultured bovine aortic endothelia and frog mesenteric capillaries

1. We have tested the hypothesis that a reduction in endothelial cell volume increases microvessel permeability and that the degree of endothelial cell attachment to their basement membranes determines the magnitude of permeability changes caused by a reduction in endothelial cell volume. 2. A decrease in endothelial cell volume was imposed on both intact microvessels and cultured endothelial monolayers by raising osmolarity by 100 mosmol 1(-1). 3. We found that hypertonic solutions did not increase the hydraulic permeability (L-p) of individually perfused venular microvessels in frog mesentery when the perfusate contained albumin. Hypertonic solutions did increase L-p, however, after we perfused the microvessels with the peptide Gly-Arg-Gly-Asp-Thr-Pro (GRGDTP; 0.3 mmol1(-1)), to disrupt integrin-dependent endothelial cell (EC) attachment to the extracellular matrix (ECM). 4. After albumin was removed from the perfusate, hypertonic solutions increased L-p of microvessels and the permeability of endothelial monolayers to alpha-lactalbumin. 5. Our findings indicate that endothelial cell integrin-ECM binding plays a role in transducing changes in cell volume and/or shape into changes in permeability. We hypothesize that removal of albumin from the vascular perfusate may compromise EC-ECM interactions via an integrin-dependent mechanism.