Editing Vasoconstriction (section)

==Causes==
Factors that trigger vasoconstriction can be exogenous or endogenous in origin. Ambient temperature is an example of exogenous vasoconstriction. Cutaneous vasoconstriction will occur because of the body's exposure to the severe cold. Examples of endogenous factors include the [[autonomic nervous system]], circulating hormones, and intrinsic mechanisms inherent to the vasculature itself (also referred to as the [[myogenic]] response).{{citation needed|date=June 2021}}

Exposure to water causes vasoconstriction near the skin, which in turn causes [[water-immersion wrinkling]].{{citation needed|date=April 2024}}

===Examples===
Examples include [[stimulants]], [[amphetamine]]s, and [[antihistamine]]s. Many are used in medicine to treat [[hypotension]] and as [[topical decongestant]]s. Vasoconstrictors are also used clinically to increase [[blood pressure]] or to reduce local blood flow. [[Local anesthetics and vasoconstrictors|Vasoconstrictors mixed with local anesthetics]] are used to increase the duration of local anesthesia by constricting the blood vessels, thereby safely concentrating the anesthetic agent for an extended duration, as well as reducing [[hemorrhage]].<ref>{{cite journal |author=Yagiela JA |title=Vasoconstrictor agents for local anesthesia |journal=Anesth Prog |volume=42 |issue=3–4 |pages=116–20 |year=1995 |pmid=8934977 |pmc=2148913}}</ref><ref>{{cite journal |last1=Moodley |first1=D. S. |title=Local anaesthetics in dentistry - Part 3: Vasoconstrictors in local anaesthetics |journal=South African Dental Journal |date=May 2017 |volume=72 |issue=4 |pages=176–178 |hdl=10566/3893 |hdl-access=free }}</ref>

The [[routes of administration]] vary. They may be both systemic and topical. For example, [[pseudoephedrine]] is taken orally and [[phenylephrine]] is topically applied to the nasal passages or eyes.<ref>{{cite journal |last1=Salerno |first1=Stephen M. |last2=Jackson |first2=Jeffrey L. |last3=Berbano |first3=Elizabeth P. |title=Effect of Oral Pseudoephedrine on Blood Pressure and Heart Rate: A Meta-analysis |journal=Archives of Internal Medicine |date=8 August 2005 |volume=165 |issue=15 |pages=1686–1694 |doi=10.1001/archinte.165.15.1686 |pmid=16087815 }}</ref><ref>{{cite journal |last1=Horak |first1=Friedrich |last2=Zieglmayer |first2=Petra |last3=Zieglmayer |first3=René |last4=Lemell |first4=Patrick |last5=Yao |first5=Ruji |last6=Staudinger |first6=Heribert |last7=Danzig |first7=Melvyn |title=A placebo-controlled study of the nasal decongestant effect of phenylephrine and pseudoephedrine in the Vienna Challenge Chamber |journal=Annals of Allergy, Asthma & Immunology |date=February 2009 |volume=102 |issue=2 |pages=116–120 |doi=10.1016/s1081-1206(10)60240-2 |pmid=19230461 }}</ref> Examples include:<ref>{{cite book |doi=10.1007/7854_2016_64 |chapter=Pharmacology and Toxicology of N-Benzylphenethylamine ('NBOMe') Hallucinogens |title=Neuropharmacology of New Psychoactive Substances (NPS) |series=Current Topics in Behavioral Neurosciences |date=2017 |last1=Halberstadt |first1=Adam L. |volume=32 |pages=283–311 |pmid=28097528 |isbn=978-3-319-52442-9 }}</ref><ref>{{cite journal |last1=Echeverri |first1=Darío |last2=Montes |first2=Félix R. |last3=Cabrera |first3=Mariana |last4=Galán |first4=Angélica |last5=Prieto |first5=Angélica |title=Caffeine's Vascular Mechanisms of Action |journal=International Journal of Vascular Medicine |date=25 August 2010 |volume=2010 |pages=1–10 |doi=10.1155/2010/834060 |pmid=21188209 |pmc=3003984 |doi-access=free }}</ref><ref>{{Cite journal |last1=Laccourreye |first1=O. |last2=Werner |first2=A. |last3=Giroud |first3=J.-P. |last4=Couloigner |first4=V. |last5=Bonfils |first5=P. |last6=Bondon-Guitton |first6=E. |date=2015 |title=Benefits, limits and danger of ephedrine and pseudoephedrine as nasal decongestants |journal=European Annals of Otorhinolaryngology, Head and Neck Diseases |volume=132 |issue=1 |pages=31–34 |doi=10.1016/j.anorl.2014.11.001 |pmid=25532441 |doi-access=free }}</ref>
{| class="wikitable"
|-
!Vasoconstrictors
|-
|[[25I-NBOMe]]
|-
|[[Amphetamine]]s
|-
|[[Alpha-Methyltryptamine|AMT]]
|-
|[[Antihistamines]]
|-
|[[Caffeine]]
|-
|[[Cocaine]]
|-
|[[2,5-Dimethoxy-4-methylamphetamine|DOM]]
|-
|[[Ergometrine]]
|-
|[[Ergine|LSA]]
|-
|[[Lysergic acid diethylamide|LSD]]
|-
|[[Methylphenidate]]
|-
|[[Mephedrone]]
|-
|[[Naphazoline]]
|-
|[[Nicotine]]<ref>{{Cite journal |last1=Hwang |first1=Kun |last2=Son |first2=Ji Soo |last3=Ryu |first3=Woo Kyung |date=November 2018 |title=Smoking and Flap Survival |journal=Plastic Surgery (Oakville, Ont.) |volume=26 |issue=4 |pages=280–285 |doi=10.1177/2292550317749509 |issn=2292-5503 |pmc=6236508 |pmid=30450347}}</ref>
|-
|[[Oxymetazoline]]
|-
|[[Phenylephrine]]
|-
|[[Propylhexedrine]]
|-
|[[Pseudoephedrine]]
|-
|[[Stimulant]]s
|-
|[[Tetrahydrozoline|Tetrahydrozoline hydrochloride]] (in eye drops)
|-
|[[Xylometazoline]]
|}

===Endogenous===
Vasoconstriction is a procedure of the body that averts [[orthostatic hypotension]]. It is part of a body [[negative feedback]] loop in which the body tries to restore homeostasis (maintain constant internal environment).{{citation needed|date=June 2021}}

For example, vasoconstriction is a hypothermic preventative in which the blood vessels constrict and blood must move at a higher pressure to actively prevent a hypoxic reaction. [[Adenosine triphosphate|ATP]] is used as a form of energy to increase this pressure to heat the body. Once homeostasis is restored, the blood pressure and ATP production regulates. Vasoconstriction also occurs in superficial blood vessels of [[warm-blooded]] animals when their ambient environment is cold; this process diverts the flow of heated blood to the center of the animal, preventing the loss of heat.{{Citation needed|date=June 2021}}

{| class="wikitable"
|-
!Vasoconstrictor<ref name=boron/>
!Receptor <br> (↑ = opens. ↓ = closes)<ref name=boron/> <br> <span style="font-size:85%;"> On [[vascular smooth muscle cells]] if not otherwise specified</span>
!Transduction <br> (↑ = increases. ↓ = decreases)<ref name=boron>Unless else specified in box, then ref is: {{cite book |author=Walter F. Boron |title=Medical Physiology: A Cellular And Molecular Approaoch |publisher=Elsevier/Saunders |year= 2005|isbn=1-4160-2328-3 }} Page 479</ref>
|-
| Stretch || ↑[[Stretch-activated ion channel]]s
|rowspan=2| [[depolarization]] -->
* open [[Voltage-dependent calcium channel|VDCC]]s (primarily) --> ↑intracellular Ca<sup>2+</sup>
* ↑Voltage-gated [[sodium channel|Na<sup>+</sup> channel]]s -->
** more depolarization --> open [[Voltage-dependent calcium channel|VDCC]]s --> ↑intracellular Ca<sup>2+</sup>
** ↓[[Sodium-calcium exchanger|Na<sup>+</sup>-Ca<sup>2+</sup> exchanger]] activity --> ↑intracellular Ca<sup>2+</sup>
|-
| [[adenosine triphosphate|ATP]] (intracellular) || ↓[[ATP-sensitive potassium channel|ATP-sensitive K<sup>+</sup> channel]]
|-
| [[adenosine triphosphate|ATP]] (extracellular) || ↑[[P2X receptor]] || ↑Ca<sup>2+</sup>
|-
|[[Neuropeptide Y|NPY]] || [[NPY receptor]]
|| Activation of [[gi alpha subunit|G<sub>i</sub>]] --> ↓[[cyclic adenosine monophosphate|cAMP]] --> ↓[[protein kinase A|PKA]] activity --> ↓[[phosphorylation]] of [[myosin light chain kinase|MLCK]] --> ↑MLCK activity --> ↑phosphorylation of [[myosin light chain|MLC]] (calcium-independent)
|-
| [[adrenergic agonists]] <br> e.g., [[epinephrine]], [[norepinephrine]], and [[dopamine]]|| ↑[[alpha-1 adrenergic receptor|α<sub>1</sub> adrenergic receptor]]
|rowspan=3| Activation of [[gq alpha subunit|G<sub>q</sub>]] --> ↑[[phospholipase C|PLC]] activity --> ↑[[Inositol triphosphate|IP<sub>3</sub>]] and [[diacylglycerol|DAG]] --> activation of [[Inositol triphosphate receptor|IP<sub>3</sub> receptor]] in [[sarcoplasmic reticulum|SR]] --> ↑intracellular Ca<sup>2+</sup>
|-
| [[thromboxane]] || ↑[[thromboxane receptor]]
|-
| [[endothelin]] || ↑[[endothelin receptor]] ET<sub>A</sub>
|-
|rowspan=2| [[angiotensin II]] || ↑[[Angiotensin receptor#AT1|Angiotensin receptor 1]]
|
* On smooth muscle cells: Activation of [[gq alpha subunit|G<sub>q</sub>]] --> ↑[[phospholipase C|PLC]] activity --> ↑[[Inositol triphosphate|IP<sub>3</sub>]] and [[diacylglycerol|DAG]] --> activation of [[Inositol triphosphate receptor|IP<sub>3</sub> receptor]] in [[sarcoplasmic reticulum|SR]] --> ↑intracellular Ca<sup>2+</sup>
* On [[endothelium]]: [[endothelin]] synthesis<ref name=lange6th/>
|-
|  || open [[Voltage-dependent calcium channel|VDCC]]s --> ↑intracellular Ca<sup>2+</sup><ref name=boron2>{{cite book |author=Walter F. Boron |title=Medical Physiology: A Cellular And Molecular Approach |publisher=Elsevier/Saunders |year= 2005|isbn=1-4160-2328-3 }} Page 771</ref>
|-
| [[Asymmetric dimethylarginine]] ||||Reduced production of [[nitric oxide]]
|-
|rowspan=2| [[Vasopressin|Antidiuretic hormone (ADH or Vasopressin)]] || [[Arginine vasopressin receptor 1]] (V1) on smooth muscle cells
| Activation of [[gq alpha subunit|G<sub>q</sub>]] --> ↑[[phospholipase C|PLC]] activity --> ↑[[Inositol triphosphate|IP<sub>3</sub>]] and [[diacylglycerol|DAG]] --> activation of [[Inositol triphosphate receptor|IP<sub>3</sub> receptor]] in [[sarcoplasmic reticulum|SR]] --> ↑intracellular Ca<sup>2+</sup>
|-
| [[Arginine vasopressin receptor]] on endothelium || [[Endothelin]] production<ref name=lange6th/>
|-
|
* Products of [[platelet activation]]<ref name=lange6th>{{cite book |author1=Rod Flower |author2=Humphrey P. Rang |author3=Maureen M. Dale |author4=Ritter, James M. |title=Rang & Dale's pharmacology |publisher=Churchill Livingstone |location=Edinburgh |year=2007 |isbn=978-0-443-06911-6 }}</ref>
* [[Endotoxin]]<ref name=lange6th/>
* [[Thrombin]]<ref name=lange6th/>
* [[insulin]]<ref name=lange6th/>
* [[Hypoxia (medical)|Hypoxia]]<ref name=lange6th/>
* Low [[shear stress]]<ref name=lange6th/>
| Various receptors on [[endothelium]]<ref name=lange6th/>  || [[Endothelin]] production<ref name=lange6th/>
|}