Vasodilation

Vasodilation, also known as vasorelaxation, is the widening of blood vessels. It results from relaxation of smooth muscle cells within the vessel walls, in particular in the large veins, large arteries, and smaller arterioles. Blood vessel walls are composed of endothelial tissue and a basal membrane lining the lumen of the vessel, concentric smooth muscle layers on top of endothelial tissue, and an adventitia over the smooth muscle layers. Relaxation of the smooth muscle layer allows the blood vessel to dilate, as it is held in a semi-constricted state by sympathetic nervous system activity. Vasodilation is the opposite of vasoconstriction, which is the narrowing of blood vessels.

When blood vessels dilate, the flow of blood is increased due to a decrease in vascular resistance and increase in cardiac output^{[further explanation needed]}. Vascular resistance is the amount of force circulating blood must overcome in order to allow perfusion of body tissues. Narrow vessels create more vascular resistance, while dilated vessels decrease vascular resistance. Vasodilation acts to increase cardiac output by decreasing afterload, −one of the four determinants of cardiac output.

By expanding available area for blood to circulate, vasodilation decreases blood pressure. The response may be intrinsic (due to local processes in the surrounding tissue) or extrinsic (due to hormones or the nervous system). In addition, the response may be localized to a specific organ (depending on the metabolic needs of a particular tissue, as during strenuous exercise), or it may be systemic (seen throughout the entire systemic circulation).

Endogenous substances and drugs that cause vasodilation are termed vasodilators. Many of these substances are neurotransmitters released by perivascular nerves of the autonomic nervous system Baroreceptors sense blood pressure and allow adaptation via the mechanisms of vasoconstriction or vasodilation to maintain homeostasis.

The primary function of vasodilation is to increase blood flow in the body to tissues that need it most. This is often in response to a localized need for oxygen but can occur when the tissue in question is not receiving enough glucose, lipids, or other nutrients. Vasodilation, both localized and systemic, also facilitates immune response. Localized tissues have multiple ways to increase blood flow, including releasing vasodilators, primarily adenosine, into the local interstitial fluid, which diffuses to capillary beds, provoking local vasodilation. Some physiologists have suggested that it is the lack of oxygen itself that causes capillary beds to vasodilate by the smooth muscle hypoxia of the vessels in the region. This latter hypothesis is posited due to the presence of precapillary sphincters in capillary beds. These approaches to the mechanism of vasodilation have not been found to be mutually exclusive.

Vasodilation plays a major role in immune system function. Wider blood vessels allow more blood containing immune cells and proteins to reach the infection site. Vasodilation occurs as part of the process of inflammation, which is caused by several factors including presence of a pathogen, injury to tissues or blood vessels, and immune complexes. In severe cases, inflammation can lead to sepsis or distributive shock. Vasodilation is also a major component of anaphylaxis.

Inflammation causes not only vasodilation but also causes increased vascular permeability, allowing neutrophils, complement proteins, and antibodies to reach the site of infection or damage. Elevated vascular permeability can allow excess fluid to leave blood vessels and collect in tissues resulting in edema; vasodilation prevents blood vessels from constricting to adapt to reduced volume in the vessels, causing low blood pressure and septic shock.

In the case of inflammation, vasodilation is caused by cytokines. Interferon gamma, TNF-a, interleukin 1 beta, and interleukin 12 are a few examples of some inflammatory cytokines produced by immune cells such as natural killer cells, B cells, T cells, mast cells and macrophages. Anti-inflammatory cytokines that regulate inflammation and help prevent negative results such as septic shock are also produced by these immune cells. Vasodilation and increased vascular permeability also allow immune effector cells to leave blood vessels and follow chemoattractants to the infection site via a process called leukocyte extravasation. Vasodilation allows the same volume of blood to move more slowly according to the flow rate equation Q = Av, where Q represents flow rate, A represents cross-sectional area, and v represents velocity. Immune effector cells can more easily attach to selectins expressed on endothelial cells when blood is flowing slowly, enabling these cells to exit the blood vessel via diapedesis.