Vascular permeability

Vascular permeability, also known as capillary permeability, refers to the capacity of blood vessels to allow for the exchange of substances between the bloodstream and the surrounding tissues. This process is crucial for the delivery of nutrients and oxygen to cells, as well as the removal of metabolic waste products. The regulation of vascular permeability is complex, involving various cellular components and signaling pathways.

Mechanisms of Vascular Permeability

Vascular permeability is primarily controlled by the endothelial cells that line the interior surface of blood vessels. These cells can form tight junctions that act as barriers to prevent the leakage of plasma proteins and other substances. However, under certain conditions, such as inflammation or in response to specific growth factors like vascular endothelial growth factor (VEGF), the permeability of these vessels can increase.

There are several mechanisms through which vascular permeability can be increased:

• Endothelial Cell Contraction: Certain mediators, such as histamine and bradykinin, can cause the endothelial cells to contract, creating gaps between the cells through which substances can pass.
• Endothelial Cell Injury: Damage to the endothelial cells, due to factors like oxidative stress or mechanical injury, can disrupt the barrier function of blood vessels.
• Transcytosis: This involves the transport of substances across the endothelial cell barrier via vesicles. It is a controlled process that can be upregulated in response to certain stimuli.
• Angiogenesis: The formation of new blood vessels can also affect vascular permeability, especially since new vessels may be more permeable than mature ones.

Regulation of Vascular Permeability

The regulation of vascular permeability involves a delicate balance between factors that increase permeability and those that decrease it. Key regulators include:

• Growth Factors: VEGF is a potent enhancer of vascular permeability. It acts by promoting endothelial cell retraction and increasing transcytosis.
• Cytokines: Pro-inflammatory cytokines, such as TNF-α and IL-1β, can increase vascular permeability by inducing changes in endothelial cell junctions.
• Nitric Oxide (NO): NO has a dual role in the regulation of vascular permeability. At low concentrations, it can enhance barrier function, while at high concentrations, it contributes to increased permeability.

Clinical Significance

Alterations in vascular permeability are associated with various pathological conditions. Increased permeability can lead to edema, the accumulation of excess fluid in tissues, which is a hallmark of inflammation. Conditions such as acute respiratory distress syndrome (ARDS), sepsis, and certain allergic reactions are characterized by significantly increased vascular permeability.

Conversely, decreased vascular permeability can impair the delivery of nutrients and oxygen to tissues, potentially leading to tissue ischemia and necrosis.

Therapeutic Implications

Understanding the mechanisms regulating vascular permeability has important therapeutic implications. For instance, drugs that stabilize endothelial cell junctions or inhibit key mediators of increased permeability, such as VEGF inhibitors, are being explored for the treatment of diseases characterized by excessive vascular leakage.

See Also

• Endothelium
• Blood-brain barrier
• Edema
• Inflammation