Vasoconstriction

Vasoconstriction
Transmission electron micrograph showing vasoconstriction of a microvessel by pericytes and endothelial cells resulting in the deformation of an erythrocyte (E).
Identifiers
MeSH	D014661
Anatomical terminology [edit on Wikidata]

Vasoconstriction is the narrowing of the blood vessels resulting from 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 blood flow. The extent of vasoconstriction may be slight or severe depending on the substance or circumstance. Many vasoconstrictors also cause pupil dilation. Medications that cause vasoconstriction include: antihistamines, decongestants, and stimulants. Severe vasoconstriction may result in symptoms of intermittent claudication.^[1]

Contents

• 
  1 General mechanism
  


• 
  2 Causes
  
  
  
  • 
    2.1 Examples
    
  
  
  • 
    2.2 Endogenous
    
  
  
  
  


• 
  3 Pathology
  


• 
  4 See also
  


• 
  5 References
  


• 
  6 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 basal level 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 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:^{[citation needed]}

Vasoconstrictors
25I-NBOMe
Amphetamines
AMT
Antihistamines
Caffeine
Cocaine
DOM
LSA
Methylphenidate
Mephedrone
Oxymetazoline
Phenylephrine
Propylhexedrine
Pseudoephedrine
Stimulants
Drugs
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.

Vasoconstrictor[4]	Receptor (↑ = opens. ↓ = closes)[4] On vascular smooth muscle cells if not otherwise specified	Transduction (↑ = increases. ↓ = decreases)[4]
Stretch	↑Stretch-activated ion channels	depolarization --> open VDCCs (primarily) --> ↑intracellular Ca2+ ↑Voltage-gated Na+ channels --> more depolarization --> open VDCCs --> ↑intracellular Ca2+ ↓Na+-Ca2+ exchanger activity --> ↑intracellular Ca2+
ATP (intracellular)	↓ATP-sensitive K+ channel
ATP (extracellular)	↑P2X receptor	↑Ca2+
NPY	NPY receptor	Activation of Gi --> ↓cAMP --> ↓PKA activity --> ↓phosphorylation of MLCK --> ↑MLCK activity --> ↑phosphorylation of MLC (calcium-independent)
adrenergic agonists e.g., epinephrine, norepinephrine, and dopamine	↑α1 adrenergic receptor	Activation of Gq --> ↑PLC activity --> ↑IP3 and DAG --> activation of IP3 receptor in SR --> ↑intracellular Ca2+
thromboxane	↑thromboxane receptor
endothelin	↑endothelin receptor ETA
angiotensin II	↑Angiotensin receptor 1	On smooth muscle cells: Activation of Gq --> ↑PLC activity --> ↑IP3 and DAG --> activation of IP3 receptor in SR --> ↑intracellular Ca2+ On endothelium: endothelin synthesis[5]
		open VDCCs --> ↑intracellular Ca2+[6]
Asymmetric dimethylarginine		Reduced production of nitric oxide
Antidiuretic hormone (ADH or Vasopressin)	Arginine vasopressin receptor 1 (V1) on smooth muscle cells	Activation of Gq --> ↑PLC activity --> ↑IP3 and DAG --> activation of IP3 receptor in SR --> ↑intracellular Ca2+
	Arginine vasopressin receptor on endothelium	Endothelin production[5]
Products of platelet activation[5] Endotoxin[5] Thrombin[5] insulin[5] Hypoxia[5] Low shear stress[5]	Various receptors on endothelium[5]	Endothelin production[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". drugs.com. Retrieved 2016-05-20..mw-parser-output cite.citation{font-style:inherit}.mw-parser-output q{quotes:"""""""'""'"}.mw-parser-output code.cs1-code{color:inherit;background:inherit;border:inherit;padding:inherit}.mw-parser-output .cs1-lock-free a{background:url("//upload.wikimedia.org/wikipedia/commons/thumb/6/65/Lock-green.svg/9px-Lock-green.svg.png")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-limited a,.mw-parser-output .cs1-lock-registration a{background:url("//upload.wikimedia.org/wikipedia/commons/thumb/d/d6/Lock-gray-alt-2.svg/9px-Lock-gray-alt-2.svg.png")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-subscription a{background:url("//upload.wikimedia.org/wikipedia/commons/thumb/a/aa/Lock-red-alt-2.svg/9px-Lock-red-alt-2.svg.png")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration{color:#555}.mw-parser-output .cs1-subscription span,.mw-parser-output .cs1-registration span{border-bottom:1px dotted;cursor:help}.mw-parser-output .cs1-hidden-error{display:none;font-size:100%}.mw-parser-output .cs1-visible-error{font-size:100%}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration,.mw-parser-output .cs1-format{font-size:95%}.mw-parser-output .cs1-kern-left,.mw-parser-output .cs1-kern-wl-left{padding-left:0.2em}.mw-parser-output .cs1-kern-right,.mw-parser-output .cs1-kern-wl-right{padding-right:0.2em}
   


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" (PDF). Biochem. J. 389 (Pt 3): 763–74. doi:10.1042/BJ20050237. PMC 1180727. PMID 15823093. Archived from the original on 2011-07-13. Retrieved 2009-07-20.
   


3. 
   ^ Yagiela JA (1995). "Vasoconstrictor agents for local anesthesia". Anesth Prog. 42 (3–4): 116–20. PMC 2148913. PMID 8934977.
   


4. 
   ^ ^abc 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. 
   ^ ^abcdefghij 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

Wikimedia Commons has media related to Vasoconstrictors.

• Definition of Vasoconstriction on HealthScout


• Cannabis arteritis revisited--ten new case reports


• Are coronary heart disease and peripheral arterial disease associated with tobacco or cannabis consumption


• Vasoconstrictor effects of Cannabis appear to inhibit Migraine (headache) attacks

v t e Physiology of the cardiovascular system
Heart	Cardiac output Cardiac cycle Cardiac output Heart rate Stroke volume Stroke volume End-diastolic volume End-systolic volume Afterload Preload Frank–Starling law Cardiac function curve Venous return curve Wiggers diagram Pressure volume diagram Ultrasound Fractional shortening = (End-diastolic dimension End-systolic dimension) / End-diastolic dimension Aortic valve area calculation Ejection fraction Cardiac index Heart rate Cardiac pacemaker Chronotropic (Heart rate) Dromotropic (Conduction velocity) Inotropic (Contractility) Bathmotropic (Excitability) Lusitropic (Relaxation) Conduction Conduction system Cardiac electrophysiology Action potential cardiac atrial ventricular Effective refractory period Pacemaker potential Electrocardiography P wave PR interval QRS complex QT interval ST segment T wave U wave Hexaxial reference system Chamber pressure Central venous Right atrial ventricular pulmonary artery wedge Left atrial ventricular Aortic Other Ventricular remodeling
Vascular system/ Hemodynamics	Blood flow Compliance Vascular resistance Pulse Perfusion Blood pressure Pulse pressure Systolic Diastolic Mean arterial pressure Jugular venous pressure Portal venous pressure Regulation of BP Baroreflex Kinin–kallikrein system Renin–angiotensin system Vasoconstrictors Vasodilators Autoregulation Myogenic mechanism Tubuloglomerular feedback Cerebral autoregulation Paraganglia Aortic body Carotid body Glomus cell

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