Hemodynamics and Barrier-Exchange Role
Endothelial cells, characterized by elongated nuclei, line the inner surface of blood vessels. At the level of the microvasculature, blood flow geometry changes: due to the minimal diameter of capillaries, erythrocytes are forced to move one after another (in single file). As the capillary transitions into a venule and its lumen expands, red blood cells begin to flow in two rows, and then the number of rows increases rapidly. The thin capillary wall allows for clear visualization of erythrocytes.
Together with the basement membrane, the endothelium isolates the blood from the interstitial environment. The integrity of this barrier is maintained by intercellular junctions:
- Interdigitations.
- Tight junctions (zonulae occludentes).
- Gap junctions (nexus).
Metabolism between the blood and tissue fluid in capillaries occurs via diffusion (through fenestrae or pores) and active transport using pinocytotic vesicles. In larger vessels, the endothelial layer is responsible for supplying nutrients to the inner tunics of the vessel wall itself.
Regulation of Hemostasis and Vascular Tone
The influence of the endothelium on blood clotting is dual and entirely depends on the state of the vessel. In an intact (uninjured) state, potent anticoagulant activity predominates. The cells synthesize prostacyclin and carry heparin (a sulfated glycosaminoglycan) on their surface. In addition, the glycocalyx possesses a negative charge that physically repels platelets. However, upon wall injury, a procoagulant program is triggered: cells release thromboplastin, initiating the coagulation cascade.
Numerous receptors for various hormones and bioactive substances are expressed on the cell surface (especially in arterioles). Ligand binding to these receptors induces the endothelium to synthesize factors that diffuse to the smooth muscle cell layer. As a result, smooth muscle cells relax or contract, altering the vascular lumen.
Immune Responses and the Mechanism of Inflammatory Edema
The endothelial lining actively participates in immune processes. Physiological lymphocyte migration—"homing"—occurs in lymphoid organs. The endothelium of postcapillary venules begins to express specific markers known as vascular addressins. Circulating lymphocytes recognize them and selectively home back to lymphoid tissue.
In an area of inflammation, the picture changes:
- Additional adhesion proteins appear on the surface of endothelial cells.
- Circulating leukocytes (primarily neutrophils) recognize these proteins, attach, and migrate into the tissues.
- Under the influence of inflammatory mediators, the cytoskeleton of endothelial cells reorganizes: they deform, becoming taller and shorter.
- Widening of the intercellular clefts leads to a sharp increase in permeability, causing fluid to rush into the tissues and result in edema.
Functions of Pericytes and Angiogenesis
Pericytes are cells surrounding the capillary from the outside, forming its external supporting framework. They participate in the production of basement membrane components and respond sensitively to humoral and neural stimuli. They can alter hemodynamics in two ways: either through active contraction of their structural elements, or by changing their own volume (releasing fluid or swelling).
Pericytes are indispensable in angiogenesis, which is triggered when tissues lack nutrients and oxygen. Endothelial cells begin to divide and migrate, forming branches. Pericytes exhibit high plasticity: during the remodeling of a capillary into a larger vessel, they can differentiate into smooth myocytes and fibroblasts. At the same time, direct contact between a pericyte and an endothelial cell inhibits the division of the latter, ensuring the stabilization of the new vessel. Pericytes also serve as an important link in inflammation, acting as intermediaries that transmit signals from tissues to the endothelium and stimulating the appearance of adhesion molecules on its surface.