Vasoconstriction 368674 226125521 2008-07-16T22:46:52Z 76.233.103.160 {{cleanup|date=December 2007}} '''Vasoconstriction''' is the narrowing of the blood vessels resulting from contracting of the muscular wall of the vessels. When blood vessels constrict, the flow of blood is restricted or slowed. It is the opposite of [[vasodialation]], the widening of blood vessels. Factors causing vasoconstriction are called '''vasoconstrictor''', also '''vasopressors''' or simply '''pressors'''. Vasoconstriction usually results in an increase of the [blood pressure]. Vasoconstriction may be slight or severe. Many vasoconstrictors also cause [[Pupillary response|pupil dilation]]. Vasoconstriction in the penis can disable males from maintaining an erection (erectile dysfunction). It may result from disease, medication, or psychological conditions. Medications that cause vasoconstriction include antihistamines, decongestants, methylphenidate (commonly used for ADHD), cough and cold combinations, pseudoephedrine, and caffeine. ==General mechanism== Vasoconstriction is mostly the result of increased intracellular concentration of [[calcium]] (Ca<sup>2+</sup>ions). However, specific mechanisms for generating an increased intracellular concentration of calcium depends on the vasoconstrictor. In any case, this calcium results in contraction of [[smooth muscle]] (see [[Smooth muscle]] for details), resulting in a constriction of the vessel. ==Factors and individual mechanisms== Factors that trigger vasoconstriction can be of exogenous origin, such as medication and endogenous as well, as a response from the body itself. Vasoconstriction can happen because of the severe heat. ===Medication=== Examples include [[amphetamine]]s, [[antihistamine]]s and [[cocaine]]. 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. The [[routes of administration]] varies. They may be both systemic and topical. For example, [[pseudoephedrine]] is available systemic (i.e. orally ingested tablets like [[Sudafed]]), and topical (such as nose sprays like phenylephrine [[Neo-synephrine]], and eye drops for [[pupil dilation]] purposes) Examples include: "Where are the &uarr; &darr; 's ?" {| class="wikitable" !Vasoconstrictor !Receptor <BR> (&uarr; = opens. &darr; = closes) !Transduction <BR> (&uarr; = increases. &darr; = decreases) |- |[[Amphetamine]]s || || |- |[[Antihistamine]]s || || |- |[[Cocaine]] || || |- |[[Caffeine]] || || |- |[[Decongestant]]s || || |- |[[Ergine]] || || |- |[[LSD]] || || |- |[[LSA]] || || |- |[[Methylphenidate]] || || |- |[[Phenylephrine]] || || |- |[[Pseudoephedrine]] || || |- |[[Stimulant]]s || || |- |[[Tetrahydrozoline|Tetrahydrozoline hydrochloride]] (in eye drops) || || |- |[[Psilocybin]] || || |- |} ===Endogenous=== Vasoconstriction is a procedure of the body that avoids orthostatic hypotension. It is a part of a body negative feed back loop in which the body tries to restore homeostasis. For example, vasoconstriction is a hypothermic preventative in which the blood vessels constrict and blood must move at a higher pressure to actively avoid 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. {| class="wikitable" !Vasoconstrictor <ref name=boron/> !Receptor <BR> (&uarr; = opens. &darr; = closes) <ref name=boron/> !Transduction <BR> (&uarr; = increases. &darr; = decreases) <ref name=boron> Unless else specified in box, then ref is: {{cite book |author=Walter F., PhD. Boron |title=Medical Physiology: A Cellular And Molecular Approaoch |publisher=Elsevier/Saunders |location= |year= |pages= |isbn=1-4160-2328-3 |oclc= |doi=}} Page 479 </ref> |- | Stretch || &uarr;[[Stretch-activated ion channel]]s |rowspan=2| [[depolarization]] --> *open [[Voltage-dependent calcium channel|VDCC]]s (primarily) --> &uarr;intracellular Ca<sup>2+</sup> *&uarr;Voltage-gated [[sodium channel|Na<sup>+</sup> channel]]s --> **more depolarization --> open [[Voltage-dependent calcium channel|VDCC]]s --> &uarr;intracellular Ca<sup>2+</sup> **&darr;[[Sodium-calcium exchanger|Na<sup>+</sup>-Ca<sup>2+</sup> exchanger]] activity --> &uarr;intracellular Ca<sup>2+</sup> |- | [[adenosine triphosphate|ATP]] (intracellular) || &darr;[[ATP-sensitive K+ channel|ATP-sensitive K<sup>+</sup> channel]] |- |- | [[muscarinic agonist]]s <BR> e.g. [[acetylcholine]] || &uarr;[[Muscarinic acetylcholine receptor M2|muscarinic receptor M<sub>2</sub>]] |rowspan=2| Activation of [[gi alpha subunit|G<sub>i</sub>]] --> &darr;[[cyclic adenosine monophosphate|cAMP]] --> &darr;[[protein kinase A|PKA]] activity --> &darr;[[phosphorylation]] of [[myosin light chain kinase|MLCK]] --> &uarr;MLCK activity --> &uarr;phosphorylation of [[myosin light chain|MLC]] (calcium-independent) |- |[[Neuropeptide Y|NPY]] || [[NPY receptor]] |- | [[adrenergic agonists]] <BR> e.g. [[norepinephrine]] || &uarr;[[alpha-1 adrenergic receptor|α<sub>1</sub> adrenergic receptor]] |rowspan=3| Activation of [[gq alpha subunit|G<sub>q</sub>]] --> &uarr;[[phospholipase C|PLC]] activity --> &uarr;[[Inositol triphosphate|IP<sub>3</sub>]] and [[diacylglycerol|DAG]] --> activation of [[Inositol triphosphate receptor|IP<sub>3</sub> receptor]] in [[sarcoplasmic reticulum|SR]] --> &uarr;intracellular Ca<sup>2+</sup> |- | [[thromboxane]] || &uarr;[[thromboxane receptor]] |- | [[endothelin]] || &uarr;[[endothelin receptor]] ET<sub>A</sub> |- |rowspan=2| [[angiotensin II]] || &uarr;[[Angiotensin_type_I_receptor#at1|Angiotensin receptor 1]] || Activation of [[gq alpha subunit|G<sub>q</sub>]] --> &uarr;[[phospholipase C|PLC]] activity --> &uarr;[[Inositol triphosphate|IP<sub>3</sub>]] and [[diacylglycerol|DAG]] --> activation of [[Inositol triphosphate receptor|IP<sub>3</sub> receptor]] in [[sarcoplasmic reticulum|SR]] --> &uarr;intracellular Ca<sup>2+</sup> |- | || open [[Voltage-dependent calcium channel|VDCC]]s --> &uarr;intracellular Ca<sup>2+</sup><ref name=boron2> {{cite book |author=Walter F., PhD. Boron |title=Medical Physiology: A Cellular And Molecular Approaoch |publisher=Elsevier/Saunders |location= |year= |pages= |isbn=1-4160-2328-3 |oclc= |doi=}} Page 771 </ref> |- | [[adenosine triphosphate|ATP]] (extracellular) || &uarr;[[P2X receptor]] || &uarr;Ca<sup>2+</sup> |- |moderately high levels of [[Stress (medicine)|stress]] || - || release of adrenergic agonists |- | [[Asymmetric dimethylarginine]] || |} ===Others=== {| class="wikitable" !Vasoconstrictor !Mechanism |- |[[Over-illumination|Bright light]] || |- |Cold (water, air, etc.) || |- |[[Noise health effects|Elevated sound levels]] || |- |} ==Pathology== Vasoconstriction can be a contributing factor to [[erectile dysfunction]].<ref>Richard Milsten and Julian Slowinski, ''The sexual [[male]]'',bc,main point W.W. Norton Company, New York, London (1999) ISBN 0-393-04740-7</ref> An increase of blood flow in the penis that builds up causes an erection, however if the body is not functioning properly the blood vessels in the penis activate and allow less blood to pool, meaning the erection goes down prematurely or simply fails to completely go up. This does not necessarily mean that the person in question is not aroused, it is a lapse in judgement between the Central Nervous System [CNS] and the Peripheral Nervous System [PNS] . When blood pools in the penis the body reacts to the excessive heat to cool it, resulting in vasoconstriction. == References== <div class="references-small"> <references /> </div> ==See also== *[[Addison's disease]] *[[Inotrope]] *[[Hypotension]] *[[Nitric oxide]] *[[Pheochromocytoma]] *[[Shock (medical)|Shock]] *[[Vasodilation]] *[[Postural orthostatic tachycardia syndrome]] ==External links== * [http://www.healthscout.com/ency/1/002338.html Definition of Vasoconstriction on HealthScout] * [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11205926&dopt=Abstract Cannabis arteritis revisited--ten new case reports] * [http://www.aegis.com/conferences/Lipo/2003/34.html Are coronary heart disease and peripheral arterial disease associated with tobacco or cannabis consumption] * [http://www.druglibrary.org/schaffer/hemp/medical/cannabin1.htm Vasoconstrictor effects of Cannabis appear to inhibit Migraine (headache) attacks] {{Cardiovascular physiology}} [[Category:Cardiovascular system]] [[Category:Drugs]] [[de:Vasokonstriktion]] [[es:Vasoconstricción]] [[fr:Vasoconstricteur]] [[it:Vasocostrittore]] [[nl:Vasoconstrictie]] [[pl:Wazokonstrykcja]] [[pt:Vasoconstrição]] [[ru:Вазоконстрикторы]] [[ru:Вазоконстрикция]] [[sr:Вазоконстрикција]] [[uk:Судинозвужуючі речовини]] [[zh:血管收縮]]