Editing Vasodilation (section)

== Function ==
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 [[dioxygen in biological reactions|need for oxygen]] but can occur when the tissue in question is not receiving enough [[glucose]], [[lipid]]s, or other [[nutrients]]. Vasodilation, both localized and systemic, also facilitates immune response.<ref name="Sprague_2009">{{cite journal | vauthors = Sprague AH, Khalil RA | title = Inflammatory cytokines in vascular dysfunction and vascular disease | journal = Biochemical Pharmacology | volume = 78 | issue = 6 | pages = 539–52 | date = September 2009 | pmid = 19413999 | pmc = 2730638 | doi = 10.1016/j.bcp.2009.04.029 }}</ref> 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.<ref name="pmid9576114">{{cite journal | vauthors = Costa F, Biaggioni I | title = Role of nitric oxide in adenosine-induced vasodilation in humans | journal = Hypertension | volume = 31 | issue = 5 | pages = 1061–1064 | date = May 1998 | pmid = 9576114 | doi = 10.1161/01.HYP.31.5.1061 | doi-access = free }}</ref><ref name="pmid15772334">{{cite journal | vauthors = Sato A, Terata K, Miura H, Toyama K, Loberiza FR, Hatoum OA, Saito T, Sakuma I, Gutterman DD | title = Mechanism of vasodilation to adenosine in coronary arterioles from patients with heart disease | journal = American Journal of Physiology. Heart and Circulatory Physiology | volume = 288 | issue = 4 | pages = H1633–H1640 | date = April 2005 | pmid = 15772334 | doi = 10.1152/ajpheart.00575.2004 | s2cid = 71178 }}</ref> Some physiologists have suggested that it is the lack of oxygen itself that causes capillary beds to vasodilate by the smooth muscle [[hypoxia (medical)|hypoxia]] of the vessels in the region.  This latter hypothesis is posited due to the presence of [[precapillary sphincter]]s in capillary beds.  These approaches to the mechanism of vasodilation have not been found to be  [[mutually exclusive]].<ref>{{cite book | vauthors = Guyton A, Hall J | veditors = Gruliow R  |title=Textbook of Medical Physiology |url=https://archive.org/details/textbookmedicalp00acgu |url-access=limited |type=Book |edition=11th |year=2006 |publisher=Elsevier Inc. |location=Philadelphia, Pennsylvania |isbn=978-0-7216-0240-0 |pages=[https://archive.org/details/textbookmedicalp00acgu/page/n230 196]–197  |chapter=Chapter 17: Local and Humoral Control of Blood Flow by the Tissues}}</ref>

=== Immune system ===
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 complex]]es.<ref name="Sprague_2009" /> In severe cases, inflammation can lead to [[sepsis]] or distributive shock.<ref name="Vincent_2013" /> Vasodilation is also a major component of [[anaphylaxis]].<ref name="Pałgan_2023">{{cite journal | vauthors = Pałgan K | title = Mast Cells and Basophils in IgE-Independent Anaphylaxis | journal = International Journal of Molecular Sciences | volume = 24 | issue = 16 | pages = 12802 | date = August 2023 | pmid = 37628983 | doi = 10.3390/ijms241612802 | doi-access = free | pmc = 10454702 }}</ref>

Inflammation causes not only vasodilation but also causes increased [[vascular permeability]], allowing [[neutrophil]]s, [[complement proteins]], and [[antibodies]] to reach the site of infection or damage.<ref name="Sprague_2009" /> 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]].<ref name="Vincent_2013" />

In the case of inflammation, vasodilation is caused by [[cytokine]]s.<ref name="Sprague_2009" /> [[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 cell]]s, [[B cell]]s, [[T cell]]s, [[mast cell]]s and [[macrophage]]s.<ref name="Sprague_2009" /> Anti-inflammatory cytokines that regulate inflammation and help prevent negative results such as septic shock are also produced by these immune cells.<ref name="Sprague_2009" /> Vasodilation and increased vascular permeability also allow immune [[effector cell]]s to leave blood vessels and follow [[chemoattractant]]s to the infection site via a process called [[leukocyte extravasation]].<ref name="Nourshargh_2014">{{cite journal | vauthors = Nourshargh S, Alon R | title = Leukocyte migration into inflamed tissues | journal = Immunity | volume = 41 | issue = 5 | pages = 694–707 | date = November 2014 | pmid = 25517612 | doi = 10.1016/j.immuni.2014.10.008 | doi-access = free }}</ref> 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.<ref>{{Cite web |title=What is volume flow rate? (article) {{!}} Fluids |url=https://www.khanacademy.org/science/physics/fluids/fluid-dynamics/a/what-is-volume-flow-rate |access-date=2024-03-23 |website=Khan Academy |language=en}}</ref> Immune effector cells can more easily attach to [[selectin]]s expressed on endothelial cells when blood is flowing slowly, enabling these cells to exit the blood vessel via [[diapedesis]].<ref name="Nourshargh_2014" />

[[Anaphylaxis]] is a severe allergic reaction characterized by elevated vascular permeability, systemic vasodilation, gastrointestinal dysfunction, and respiratory dysfunction.<ref>{{cite journal | vauthors = Nguyen SM, Rupprecht CP, Haque A, Pattanaik D, Yusin J, Krishnaswamy G | title = Mechanisms Governing Anaphylaxis: Inflammatory Cells, Mediators, Endothelial Gap Junctions and Beyond | journal = International Journal of Molecular Sciences | volume = 22 | issue = 15 | pages = 7785 | date = July 2021 | pmid = 34360549 | doi = 10.3390/ijms22157785 | doi-access = free | pmc = 8346007 }}</ref> [[Anaphylatoxin]]s, specifically [[complement protein]]s C3a and C5a, bind to receptors on mast cells and basophils causing [[degranulation]].<ref name="Pałgan_2023" /> Granules in these cells contain [[histamine]], [[platelet-activating factor]], and other compounds causing clinical manifestation of anaphylaxis- including systemic vasodilation causing dangerously low blood pressure.<ref name="Pałgan_2023" /> [[Immunoglobulin E]], an antibody produced by [[plasma cell]]s, also binds to receptors on mast cells and basophils causing degranulation.<ref name="Pałgan_2023" />