Vasoconstriction
Vasoconstriction | |
---|---|
erythrocyte (E). | |
Identifiers | |
MeSH | D014661 |
Anatomical terminology] |
Vasoconstriction is the narrowing of the
Medications causing vasoconstriction, also known as vasoconstrictors, are one type of
General mechanism
The mechanism that leads to vasoconstriction results from the increased concentration of
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.[citation needed]
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
Exposure to water causes vasoconstriction near the skin, which in turn causes
Examples
Examples include
The
Vasoconstrictors |
---|
25I-NBOMe |
Amphetamines |
AMT
|
Antihistamines
|
Caffeine |
Cocaine |
DOM |
Ergometrine |
LSA |
LSD
|
Methylphenidate |
Mephedrone |
Naphazoline |
Oxymetazoline |
Phenylephrine |
Propylhexedrine |
Pseudoephedrine |
Stimulants |
Tetrahydrozoline hydrochloride (in eye drops)
|
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]
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.[citation needed]
Vasoconstrictor[11] | Receptor (↑ = opens. ↓ = closes) vascular smooth muscle cells if not otherwise specified
|
Transduction (↑ = increases. ↓ = decreases)[11] |
---|---|---|
Stretch | ↑ Stretch-activated ion channels
|
depolarization -->
|
ATP (intracellular) | ↓ATP-sensitive K+ channel | |
ATP (extracellular) | ↑ P2X receptor |
↑Ca2+ |
NPY | NPY receptor
|
Activation of MLCK --> ↑MLCK activity --> ↑phosphorylation of MLC (calcium-independent)
|
epinephrine, norepinephrine, and dopamine |
↑α1 adrenergic receptor | Activation of IP3 receptor in SR --> ↑intracellular Ca2+
|
thromboxane | ↑thromboxane receptor | |
endothelin | ↑endothelin receptor ETA | |
angiotensin II |
↑ Angiotensin receptor 1
|
|
open VDCCs --> ↑intracellular Ca2+[13]
| ||
Asymmetric dimethylarginine | Reduced production of nitric oxide | |
Antidiuretic hormone (ADH or Vasopressin) | Arginine vasopressin receptor 1 (V1) on smooth muscle cells
|
Activation of IP3 receptor in SR --> ↑intracellular Ca2+
|
Arginine vasopressin receptor on endothelium |
Endothelin production[12] | |
Various receptors on endothelium[12] | Endothelin production[12] |
Pathology
Vasoconstriction can be a contributing factor to erectile dysfunction.[14] An increase in blood flow to the penis causes an erection.
Improper vasoconstriction may also play a role in secondary hypertension.[citation needed]
To summarize, vasoconstriction is a physiological process that involves the narrowing of blood vessels, particularly arteries and arterioles, resulting in a reduction of blood flow to specific tissues or organs. This phenomenon is primarily regulated by the contraction of smooth muscle cells within the vessel walls. Several factors contribute to vasoconstriction, including the release of vasoconstrictor substances such as endothelin and angiotensin II, both of which play crucial roles in the modulation of vascular tone.[15]
Additionally, sympathetic nervous system activation, triggered by stress or other stimuli, prompts the release of norepinephrine, a neurotransmitter that induces vasoconstriction by binding to alpha-adrenergic receptors on smooth muscle cells. The narrowing of blood vessels leads to an increase in peripheral resistance, thereby elevating blood pressure. While vasoconstriction is a normal and essential regulatory mechanism for maintaining blood pressure and redistributing blood flow during various physiological processes, its dysregulation can contribute to pathological conditions. Chronic vasoconstriction is associated with hypertension, a major risk factor for cardiovascular diseases such as heart attack and stroke. Moreover, impaired blood flow resulting from abnormal vasoconstriction may contribute to tissue ischemia, which can be observed in conditions like Raynaud's disease. Understanding the pathology of vasoconstriction is crucial for developing targeted therapeutic strategies to manage conditions associated with abnormal vascular tone.[16]
See also
References
- ^ "Medihaler Ergotamine". drugs.com. Retrieved 2016-05-20.
- ^
Michael P. Walsh; et al. (2005-08-01) [Published on Journal website 2005-07-26]. "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". Biochem J. 389 (3): 763–774. PMID 15823093.
These results suggest that U-46619 elicits contraction of rat caudal arterial smooth muscle by activating Ca2+ entry from the extracellular space, which may or may not involve Ca2+-induced Ca2+ release from the SR (sarcoplasmic reticulum). … A key step in the contractile response to U-46619 appears to be the entry of extracellular Ca2+, since it was abolished by removal of extracellular Ca2+ (Figure 2A). … In the rat caudal artery, U-46619-mediated contractile responses have an absolute requirement for Ca2+, which enters from the extracellular pool, is independent of intracellular Ca2+ stores and is blocked by ROK inhibition.
- PMID 9887963.
- PMID 8934977.
- hdl:10566/3893.
- PMID 16087815.
- PMID 19230461.
- PMID 28097528.
- PMID 21188209.
- PMID 25532441.
- ^ ISBN 1-4160-2328-3. Page 479
- ^ ISBN 978-0-443-06911-6.
- ISBN 1-4160-2328-3. Page 771
- ISBN 0-393-04740-7
- PMID 23795729.
- PMID 27311222.
External links
- Definition of Vasoconstriction on HealthScout
- Disdier, Patrick; Granel, Brigitte; Serratrice, Jacques; Constans, Joël; Michon-Pasturel, Ulrique; Hachulla, Eric; Conri, Claude; Devulder, Bernard; Swiader, Laure; Piquet, Philippe; Branchereau, Alain; Jouglard, Jacqueline; Moulin, Guy; Weiller, Pierre-Jean (January 2001). "Cannabis Arteritis Revisited: Ten New Case Reports". Angiology. 52 (1): 1–5. S2CID 26030253.
- Are coronary heart disease and peripheral arterial disease associated with tobacco or cannabis consumption