Vasoconstriction

Vasoconstriction is the narrowing of the blood vessels resulting from

Vasoconstriction
contraction of the muscular wall of the vessels, in particular the large arteries
and small arterioles. The process is the opposite of vasodilation, the
widening of blood vessels. The process is particularly important in
staunching hemorrhage and acute blood loss. When blood vessels constrict,
the flow of blood is restricted or decreased, thus retaining body heat or
increasing vascular resistance. This makes the skin turn paler because less
blood reaches the surface, reducing the radiation of heat. On a larger level,
vasoconstriction is one mechanism by which the body regulates and
maintains mean arterial pressure.

Medications causing vasoconstriction, also known as vasoconstrictors, are

one type of medicine used to raise blood pressure. Generalized
vasoconstriction usually results in an increase in systemic blood pressure,
but it may also occur in specific tissues, causing a localized reduction in Transmission electron micrograph
blood flow. The extent of vasoconstriction may be slight or severe showing vasoconstriction of a
depending on the substance or circumstance. Many vasoconstrictors also microvessel by pericytes and
cause pupil dilation. Medications that cause vasoconstriction include: endothelial cells resulting in the
antihistamines, decongestants, and stimulants. Severe vasoconstriction may deformation of an erythrocyte (E).
result in symptoms of intermittent claudication.[1]
Identifiers
MeSH D014661 (https://meshb.nlm.ni
h.gov/record/ui?ui=D014661)
Contents Anatomical terminology
General mechanism
Causes
Examples
Endogenous
Pathology
See also
References
External links

General mechanism
The mechanism that leads to vasoconstriction results from the increased concentration of calcium (Ca2+ ions) within vascular
smooth muscle cells.[2] However, the specific mechanisms for generating an increased intracellular concentration of calcium
depends on the vasoconstrictor. Smooth muscle cells are capable of generating action potentials, but this mechanism is rarely
utilized for contraction in the vasculature. Hormonal or pharmacokinetic components are more physiologically relevant. Two
common stimuli for eliciting smooth muscle contraction are circulating epinephrine and activation of the sympathetic nervous
system (through release of norepinephrine) that directly innervates the muscle. These compounds interact with cell surface
adrenergic receptors. Such stimuli result in a signal transduction cascade that leads to increased intracellular calcium from the
sarcoplasmic reticulum through IP3-mediated calcium release, as well as enhanced calcium entry across the sarcolemma through
calcium channels. The rise in intracellular calcium complexes with calmodulin, which in turn activates myosin light-chain kinase.
This enzyme is responsible for phosphorylating the light chain of myosin to stimulate cross-bridge cycling.

Once elevated, the intracellular calcium concentration is returned to its normal concentration through a variety of protein pumps
and calcium exchangers located on the plasma membrane and sarcoplasmic reticulum. This reduction in calcium removes the
stimulus necessary for contraction, allowing for a return to baseline.

Causes
Factors that trigger vasoconstriction can be of exogenous or endogenous origin. Ambient temperature is an example of the
former. 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).

Examples
Examples include stimulants, amphetamines, antihistamines and cocaine. Many are used in medicine to treat hypotension and as
topical decongestants. Vasoconstrictors are also used clinically to increase blood pressure or to reduce local blood flow.
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.[3]

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.

Examples include:

Vasoconstrictors
25I-NBOMe
Amphetamines
AMT
Antihistamines
Caffeine
Cocaine
DOM
LSA
LSD
Methylphenidate
Mephedrone
Oxymetazoline
Phenylephrine
Propylhexedrine
Pseudoephedrine
Stimulants
Tetrahydrozoline hydrochloride (in eye drops)
Endogenous
Vasoconstriction is a procedure of the body that averts orthostatic hypotension. It is a part of a body negative feedback loop in
which the body tries to restore homeostasis (maintain constant internal environment).

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. 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.
 Receptor
(↑ = opens. ↓ =
closes)[4] Transduction
Vasoconstrictor[4]
On vascular smooth (↑ = increases. ↓ = decreases)[4]
muscle cells if not
otherwise specified

depolarization -->
↑Stretch-activated ion
Stretch
channels open VDCCs (primarily) --> ↑intracellular Ca2+
↑Voltage-gated Na+ channels -->

more depolarization --> open VDCCs --> ↑intracellular

ATP (intracellular) ↓ATP-sensitive K+ Ca2+
channel
↓Na+-Ca2+ exchanger activity --> ↑intracellular Ca2+

ATP (extracellular) ↑P2X receptor ↑Ca2+

Activation of Gi --> ↓cAMP --> ↓PKA activity -->
NPY NPY receptor ↓phosphorylation of MLCK --> ↑MLCK activity -->
↑phosphorylation of MLC (calcium-independent)
adrenergic agonists
e.g., epinephrine,
↑α1 adrenergic receptor
norepinephrine,
and dopamine Activation of Gq --> ↑PLC activity --> ↑IP3 and DAG -->
activation of IP3 receptor in SR --> ↑intracellular Ca2+
thromboxane ↑thromboxane receptor
endothelin ↑endothelin receptor ETA

On smooth muscle cells: Activation of Gq --> ↑PLC activity -

↑Angiotensin receptor 1 -> ↑IP3 and DAG --> activation of IP3 receptor in SR -->
angiotensin II ↑intracellular Ca2+
On endothelium: endothelin synthesis[5]

open VDCCs --> ↑intracellular Ca2+[6]

Asymmetric
Reduced production of nitric oxide
dimethylarginine
Arginine vasopressin Activation of Gq --> ↑PLC activity --> ↑IP3 and DAG -->
Antidiuretic receptor 1 (V1) on
activation of IP3 receptor in SR --> ↑intracellular Ca2+
hormone (ADH or smooth muscle cells
Vasopressin) Arginine vasopressin
Endothelin production[5]
receptor on endothelium

Products of
platelet
activation[5]
Endotoxin[5]
Various receptors on
Thrombin[5] Endothelin production[5]
endothelium[5]
insulin[5]
Hypoxia[5]
Low shear
stress[5]

Pathology
Vasoconstriction can be a contributing factor to erectile dysfunction.[7] An increase in blood flow to the penis causes an erection.
Improper vasoconstriction may also play a role in secondary hypertension.

See also
Addison's disease
Inotrope
Hypertension
Nitric oxide
Pheochromocytoma
Shock
Vasodilation
Postural orthostatic tachycardia syndrome
Hemostasis

References
1. "Medihaler Ergotamine" (https://www.drugs.com/pro/medihaler-ergotamine.html). drugs.com. Retrieved
2016-05-20.
2. Michael P. Walsh; et all (August 2005). "Thromboxane A2-induced contraction of rat caudal arterial smooth
muscle involves activation of Ca2+ entry and Ca2+sensitization: Rho-associated kinase-mediated
phosphorylation of MYPT1 at Thr-855 but not Thr-697" (https://web.archive.org/web/20110713204304/http://bios
upport.licor.com/docs/2005/BJ20050237.pdf) (PDF). Biochem. J. 389 (Pt 3): 763–74. doi:10.1042/BJ20050237 (h
ttps://doi.org/10.1042%2FBJ20050237). PMC 1180727
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1180727). PMID 15823093 (https://www.ncbi.nlm.nih.gov/pubme
d/15823093). Archived from the original (http://www.biochemj.org/content/389/3/763) on 2011-07-13. Retrieved
2009-07-20.
3. Yagiela JA (1995). "Vasoconstrictor agents for local anesthesia" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2
148913). Anesth Prog. 42 (3–4): 116–20. PMC 2148913 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC214891
3). PMID 8934977 (https://www.ncbi.nlm.nih.gov/pubmed/8934977).
4. Unless else specified in box, then ref is: Walter F. Boron. Medical Physiology: A Cellular And Molecular
Approaoch. Elsevier/Saunders. ISBN 1-4160-2328-3. Page 479
5. Rod Flower; Humphrey P. Rang; Maureen M. Dale; Ritter, James M. (2007). Rang & Dale's pharmacology.
Edinburgh: Churchill Livingstone. ISBN 0-443-06911-5.
6. Walter F. Boron. Medical Physiology: A Cellular And Molecular Approach. Elsevier/Saunders. ISBN 1-4160-2328-
3. Page 771
7. Richard Milsten and Julian Slowinski, The sexual male, bc, main point W.W. Norton Company, New York, London
(1999) ISBN 0-393-04740-7

External links
Definition of Vasoconstriction on HealthScout (https://web.archive.org/web/20071228233918/http://www.healthsc
out.com/ency/1/002338.html)
Cannabis arteritis revisited--ten new case reports (https://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&
db=PubMed&list_uids=11205926&dopt=Abstract)
Are coronary heart disease and peripheral arterial disease associated with tobacco or cannabis consumption (htt
ps://web.archive.org/web/20071209115724/http://www.aegis.com/conferences/Lipo/2003/34.html)
Vasoconstrictor effects of Cannabis appear to inhibit Migraine (headache) attacks (http://www.druglibrary.org/sch
affer/hemp/medical/cannabin1.htm)

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This page was last edited on 26 April 2019, at 14:47 (UTC).

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