TABLE Summary of Endothelial Cell Properties and Functions 13.2 Major Properties Associated Functions Active Molecules Involved Maintenance of selective permeability barrier Simple diffusion Active transport Pinocytosis Receptor-mediated endocytosis Oxygen, carbon dioxide Glucose, amino acids, electrolytes Water, small molecules, soluble  proteins LDL, cholesterol, transferrin, growth factors, antibodies, MHC complexes Maintenance of nonthrombogenic barrier Secretion of anticoagulants Secretion of antithrombogenic agents Secretion of prothrombogenic agents Thrombomodulin Prostacyclin (PGI2), tissue plasminogen activator (TPA),  antithrombin III, heparin Tissue thromboplastin, von  Willebrand factor, plasminogenactivator inhibitor Modulation of blood flow and vascular resistance Secretion of vasoconstrictors Secretion of vasodilators Endothelin, angiotensin-converting enzyme (ACE) Endothelial-derived relaxation factor (EDRF)/nitric oxide (NO),  prostacyclin Regulation of cell growth Secretion of growth-stimulating factors Secretion of growth-inhibiting factors Platelet-derived growth factor (PDGF), hemopoietic colony-stimulating factors (GM-CSF, G-CSF,   M-CSF) Heparin, transforming growth factor (TGF-) Regulation of immune responses Regulation of leukocyte migration by expression of adhesion molecules Regulation of immune functions Selectins, integrins, CD marker molecules Interleukin molecules (IL-1, IL-6, IL-8), MHC molecules Maintenance of extracellular matrix Synthesis of basal lamina Synthesis of glycocalyx Type IV collagen, laminin Proteoglycans Involvement in lipoprotein, cholesterol, metabolism Production of free radicals Oxidation of LDL Reactive oxygen species (ROS), LDL, VLDL Modified from Cotran S, Kumar V, Collins T, Robbins SL, eds. Robbins Pathologic Basis of Disease. Philadelphia: WB Saunders, 1999.
It acts as an anti-inflammatory agent under normal physiologic conditions, although its overproduction induces inflammation. NO is also involved in  immune reactions (it stimulates macrophages to release high concentrations of NO), is a potent neurotransmitter in the nervous system, and contributes to the regulation of apoptosis. The pathogenesis of inflammatory disorders of the joint, gut, and lungs is linked to local overproduction of NO. Recently, NO inhibitors have been used to manage inflammatory diseases.
Metabolic stress in endothelial cells also contributes to smooth muscle relaxation. Endothelium-derived relaxing factors include prostacyclin (PGI2), which in addition to relaxing smooth muscles is a potent inhibitor of platelet aggregation. PGI2 binds to receptors on the smooth muscles; stimulates cAMP-activated protein kinase A (PKA), which in turn phosphylates myosin light chain kinase (MLCK); and prevents activation of the calcium– calmodulin complex. This type of relaxation occurs without change in the intracellular Ca2 concentration.
represents another endothelium-derived relaxing factor that acts on Ca2-dependent potassium channels causing hyperpolarization of smooth muscle cells and their relaxation (see Fig 13.12).
Endothelins produced by vascular endothelial cells play an important role in both physiologic and pathologic mechanisms of the circulatory system.