Endothelial cells participate in the structural and functional integrity of the vascular wall.
Endothelial cells are active participants in a variety of interactions between the blood and underlying connective tissue and are responsible for many properties of the vessels (Table 13.2). These properties include the following.
 The maintenance of a selective permeability barrier allows selective movement of small and large molecules from the blood to the tissues and from the tissues to the blood. This movement is related to the size and charge of the molecules. The endothelium is permeable to small hydrophobic (lipid-soluble) molecules (e.g., oxygen, carbon dioxide) that readily pass through the lipid bilayer of the endothelial cell membrane (a process called simple diffusion). However, water and hydrophilic (water-soluble) molecules (e.g., glucose, amino acids, electrolytes) cannot diffuse across the endothelial cell membrane. These molecules and solutes must be either actively transported across the plasma membrane and released into the extracellular space (transcellular pathways) or transported across the zonula occludens between two epithelial cells (paracellular pathway; see Chapter 5, Epithelial Tissue, page 125). The transcellular pathway uses numerous small pinocytotic vesicles (a clathrin-independent form of endocytosis) to transport bulk material from the blood into the cell. In addition, some specific molecules (e.g., LDL, cholesterol, transferrin) are transported via receptor-mediated endocytosis (a clathrin-dependent process), which uses endothelial-specific surface receptors. In some blood vessels, larger molecules are transported through fenestrations within the endothelial cells visible in transmission electron microscope (TEM) preparations.
 The maintenance of a nonthrombogenic barrier between blood platelets and subendothelial tissue is done by producing anticoagulants (agents that prevent coagulation such as thrombomodulin and others) and antithrombogenic substances (agents that prevent or interfere with platelet aggregation and release of factors that cause formation of clots, or thrombi, such as prostacyclin [PGI2] and tissue plasminogen activator). Normal endothelium does not support the adherence of platelets or the formation of thrombi on its surface. Damage to endothelial cells causes them to release prothrombogenic agents (agents that promote thombi formation) such as von Willebrand factor or plasminogen-activator inhibitor.
 The modulation of blood ﬂow and vascular resistance is achieved by the secretion of vasoconstrictors (endothelins, angiotensin-converting enzyme [ACE], prostaglandin H2, thromboxane A2) and vasodilators (nitrous oxide [NO], prostacyclin). This subject is discussed in more depth in the next section.
 The regulation and modulation of immune responses is done by controlling the interaction of lymphocytes with the endothelial surface, which is mainly achieved through the expression of adhesion molecules and their receptors on the endothelial-free surface as well as by secretion of three classes of interleukins (IL-1, IL-6, and IL-8).
 Hormonal synthesis and other metabolic activities are done by the synthesis and secretion of various growth factors—for example, hemopoietic colony-stimulating factors (CSFs) such as granulocyte–macrophage CSF (GM-CSF), granulocyte CSF (G-CSF), and macrophage CSF (M-CSF); fibroblast growth factor (FGF); and platelet-derived growth factor (PDGF). Endothelial cells also synthesize growth inhibitors such as heparin and