Editing Blood vessel (section)

=== Constriction ===
{{Main|Vasoconstriction}}
[[File:Microvessel.jpg|thumb|[[Transmission electron micrograph]] of a [[microvessel]] displaying an [[erythrocyte]] (E) within its [[lumen (anatomy)|lumen]] which is deformed due to vasoconstriction]]
Arteries—and veins to a degree—can regulate their inner diameter by contraction of the muscular layer. This changes the blood flow to downstream organs and is determined by the [[autonomic nervous system]]. Vasodilation and vasoconstriction are also used antagonistically as methods of [[thermoregulation]].<ref>{{cite journal | vauthors = Charkoudian N | title = Mechanisms and modifiers of reflex induced cutaneous vasodilation and vasoconstriction in humans | journal = Journal of Applied Physiology | volume = 109 | issue = 4 | pages = 1221–1228 | date = October 2010 | pmid = 20448028 | pmc = 2963327 | doi = 10.1152/japplphysiol.00298.2010 }}</ref>

The size of blood vessels is different for each of them. It ranges from a diameter of about 30–25 millimeters for the [[aorta]]<ref>{{Cite journal |last1=Erbel |first1=Raimund |last2=Eggebrecht |first2=Holger |date=2006 |title=Aortic dimensions and the risk of dissection |journal=Heart |language=en |volume=92 |issue=1 |pages=137–142 |doi=10.1136/hrt.2004.055111 |pmc=1861012 |pmid=16365370 |quote=The normal diameter of the abdominal aorta is regarded to be less than 3.0 cm.}}</ref> to only about 5 micrometers (0,005{{Nbsp}}mm) for the capillaries.<ref>{{Cite journal |last1=Potter |first1=R. F. |last2=Groom |first2=A. C. |date=1983 |title=Capillary diameter and geometry in cardiac and skeletal muscle studied by means of corrosion casts |url=https://pubmed.ncbi.nlm.nih.gov/6835100 |journal=Microvascular Research |volume=25 |issue=1 |pages=68–84 |doi=10.1016/0026-2862(83)90044-4 |issn=0026-2862 |pmid=6835100}}</ref> Vasoconstriction is the constriction of blood vessels (narrowing, becoming smaller in cross-sectional area) by contracting the [[vascular smooth muscle]] in the vessel walls. It is regulated by [[vasoconstrictor]]s (agents that cause vasoconstriction). These can include [[paracrine]] factors (e.g., [[prostaglandin]]s), a number of [[hormone]]s (e.g., [[Antidiuretic hormone|vasopressin]] and [[angiotensin]]<ref>{{Cite journal |last1=Kanaide |first1=Hideo |last2=Ichiki |first2=Toshihiro |last3=Nishimura |first3=Junji |last4=Hirano |first4=Katsuya |date=2003-11-28 |title=Cellular Mechanism of Vasoconstriction Induced by Angiotensin II |url=https://dx.doi.org/10.1161/01.res.0000105920.33926.60 |journal=Circulation Research |volume=93 |issue=11 |pages=1015–1017 |doi=10.1161/01.res.0000105920.33926.60 |pmid=14645130 |issn=0009-7330}}</ref>) and [[neurotransmitter]]s (e.g., [[epinephrine]]) from the nervous system.

[[Vasodilation]] is a similar process mediated by antagonistically acting mediators. The most prominent vasodilator is [[nitric oxide]] (termed [[endothelium-derived relaxing factor]] for this reason).<ref>{{Cite journal |last=Cooke |first=John P |date=2000 |title=The endothelium: a new target for therapy |url=https://journals.sagepub.com/doi/10.1177/1358836X0000500108 |journal=Vascular Medicine |language=en |volume=5 |issue=1 |pages=49–53 |doi=10.1177/1358836X0000500108 |pmid=10737156 |issn=1358-863X}}</ref>