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Vasoconstriction - Wikipedia, the free encyclopedia

Vasoconstriction

From Wikipedia, the free encyclopedia

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 vasodilation, 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 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.

Contents

[edit] General mechanism

Vasoconstriction is mostly the result of increased intracellular concentration of calcium (Ca2+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.

[edit] 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.

[edit] Medication

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.

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 ↑ ↓ 's ?"

Vasoconstrictor Receptor
(↑ = opens. ↓ = closes)
Transduction
(↑ = increases. ↓ = decreases)
Amphetamines
Antihistamines
Cocaine
Caffeine
Decongestants
Ergine
LSD
LSA
Methylphenidate
Phenylephrine
Pseudoephedrine
Stimulants
Tetrahydrozoline hydrochloride (in eye drops)
Psilocybin

[edit] 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. 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 [1] Receptor
(↑ = opens. ↓ = closes) [1]
Transduction
(↑ = increases. ↓ = decreases) [1]
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
muscarinic agonists
e.g. acetylcholine
muscarinic receptor M2 Activation of Gi --> ↓cAMP --> ↓PKA activity --> ↓phosphorylation of MLCK --> ↑MLCK activity --> ↑phosphorylation of MLC (calcium-independent)
NPY NPY receptor
adrenergic agonists
e.g. norepinephrine
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

Activation of Gq --> ↑PLC activity --> ↑IP3 and DAG --> activation of IP3 receptor in SR --> ↑intracellular Ca2+

open VDCCs --> ↑intracellular Ca2+[2]
ATP (extracellular) P2X receptor ↑Ca2+
moderately high levels of stress - release of adrenergic agonists
Asymmetric dimethylarginine

[edit] Others

Vasoconstrictor Mechanism
Bright light
Cold (water, air, etc.)
Elevated sound levels

[edit] Pathology

Vasoconstriction can be a contributing factor to erectile dysfunction.[3]

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.

[edit] References

  1. ^ a b c Unless else specified in box, then ref is: Walter F., PhD. Boron. Medical Physiology: A Cellular And Molecular Approaoch. Elsevier/Saunders. ISBN 1-4160-2328-3.  Page 479
  2. ^ Walter F., PhD. Boron. Medical Physiology: A Cellular And Molecular Approaoch. Elsevier/Saunders. ISBN 1-4160-2328-3.  Page 771
  3. ^ Richard Milsten and Julian Slowinski, The sexual male,bc,main point W.W. Norton Company, New York, London (1999) ISBN 0-393-04740-7

[edit] See also

[edit] External links


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