Vascular permeability: Difference between revisions

Latest revision as of 01:00, 17 February 2025

Vascular Permeability[edit]

Vascular permeability refers to the capacity of blood vessel walls to allow the flow of small molecules (such as ions, nutrients, and water) or even whole cells (such as lymphocytes) in and out of the vessel. This process is crucial for maintaining tissue homeostasis and is involved in various physiological and pathological processes.

Mechanism[edit]

Vascular permeability is primarily regulated by the endothelial cells that line the interior surface of blood vessels. These cells form a barrier that controls the passage of substances. The permeability of this barrier can be modulated by various factors, including inflammatory cytokines, growth factors, and shear stress.

The tight junctions and adherens junctions between endothelial cells play a significant role in maintaining the integrity of the vascular barrier. Disruption of these junctions can lead to increased permeability.

Physiological Role[edit]

In normal physiology, vascular permeability is essential for the delivery of nutrients and oxygen to tissues and the removal of waste products. It also plays a role in the immune response by allowing immune cells to exit the bloodstream and enter tissues where they are needed.

Pathological Conditions[edit]

Increased vascular permeability is a hallmark of several pathological conditions, including inflammation, tumor growth, and edema. In inflammation, for example, increased permeability allows immune cells to access the site of infection or injury. However, excessive permeability can lead to tissue damage and contribute to disease progression.

Enhanced Permeability and Retention (EPR) Effect[edit]

The Enhanced Permeability and Retention (EPR) effect is a phenomenon observed in tumor biology where the leaky vasculature of tumors allows for the accumulation of macromolecules and nanoparticles. This effect is exploited in the design of nanomedicines for targeted drug delivery to tumors.

Related Pages[edit]

References[edit]

Jain, R. K. (1987). Transport of molecules in the tumor interstitium: a review. *Cancer Research*, 47(12), 3039-3051.
Maeda, H., Wu, J., Sawa, T., Matsumura, Y., & Hori, K. (2000). Tumor vascular permeability and the EPR effect in macromolecular therapeutics: a review. *Journal of Controlled Release*, 65(1-2), 271-284.

@@ Line 1: / Line 1: @@
-'''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.
+== Vascular Permeability ==
-==Mechanisms of Vascular Permeability==
+[[File:Enhanced_permeability_and_retention_(EPR)_effect.png|thumb|Illustration of the Enhanced Permeability and Retention (EPR) effect.]]
-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:
+'''Vascular permeability''' refers to the capacity of blood vessel walls to allow the flow of small molecules (such as ions, nutrients, and water) or even whole cells (such as lymphocytes) in and out of the vessel. This process is crucial for maintaining tissue homeostasis and is involved in various physiological and pathological processes.
-* '''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==
+== Mechanism ==
-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==
+Vascular permeability is primarily regulated by the [[endothelial cells]] that line the interior surface of blood vessels. These cells form a barrier that controls the passage of substances. The permeability of this barrier can be modulated by various factors, including [[inflammatory cytokines]], [[growth factors]], and [[shear stress]].
-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.
+The [[tight junctions]] and [[adherens junctions]] between endothelial cells play a significant role in maintaining the integrity of the vascular barrier. Disruption of these junctions can lead to increased permeability.
-==Therapeutic Implications==
+== Physiological Role ==
-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==
+In normal physiology, vascular permeability is essential for the delivery of nutrients and oxygen to tissues and the removal of waste products. It also plays a role in the immune response by allowing immune cells to exit the bloodstream and enter tissues where they are needed.
-* [[Endothelium]]
-* [[Blood-brain barrier]]
+== Pathological Conditions ==
-* [[Edema]]
+Increased vascular permeability is a hallmark of several pathological conditions, including [[inflammation]], [[tumor growth]], and [[edema]]. In inflammation, for example, increased permeability allows immune cells to access the site of infection or injury. However, excessive permeability can lead to tissue damage and contribute to disease progression.
+== Enhanced Permeability and Retention (EPR) Effect ==
+The Enhanced Permeability and Retention (EPR) effect is a phenomenon observed in [[tumor biology]] where the leaky vasculature of tumors allows for the accumulation of macromolecules and nanoparticles. This effect is exploited in the design of [[nanomedicine]]s for targeted drug delivery to tumors.
+== Related Pages ==
+* [[Endothelial cell]]
 * [[Inflammation]]
+* [[Tumor biology]]
+* [[Nanomedicine]]
+== References ==
-[[Category:Cardiovascular physiology]]
+* Jain, R. K. (1987). Transport of molecules in the tumor interstitium: a review. *Cancer Research*, 47(12), 3039-3051.
-[[Category:Pathophysiology]]
+* Maeda, H., Wu, J., Sawa, T., Matsumura, Y., & Hori, K. (2000). Tumor vascular permeability and the EPR effect in macromolecular therapeutics: a review. *Journal of Controlled Release*, 65(1-2), 271-284.
-{{Medicine-stub}}
+[[Category:Vascular biology]]
+[[Category:Physiology]]
+<gallery>
+File:Enhanced_permeability_and_retention_(EPR)_effect.png
+</gallery>