Endothelial permeability is in large part regulated by intercellular junctions. These are complex structures formed by transmembrane adhesive molecules linked to a network of cytoskeletal proteins. At least four types of endothelial junctions have been described {tight, gap and adherence junctions and complexus adherentes). These organelles have some features and components in common with epithelial cells but also some which are specific for the endothelium. The mechanisms that regulate the opening and closing of endothelial junctions are still obscure. Inflammatory agents increase permeabilty by binding to specific receptors and generating intracellular signals which in turn cause cytoskeletal reorganization and opening of interendothelial cell gaps. Endothelial junctions also control leukocyte extravasation. Once leukocytes have adhered to the endothelium, a coordinated opening of interendothelial cell junctions occurs. The mechanism by which this takes place presents characteristics similar to that triggered by soluble mediators.