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Vasodilation refers to the widening of blood vessels[1] resulting from relaxation of smooth muscle cells within the vessel walls, particularly in the large arteries, smaller arterioles and large veins. The process is essentially the opposite of vasoconstriction, or the narrowing of blood vessels. When vessels dilate, the flow of blood is increased due to a decrease in vascular resistance. Therefore, dilation of arterial blood vessels (mainly arterioles) leads to a decrease in blood pressure. The response may be intrinsic (due to local processes in the surrounding tissue) or extrinsic (due to hormones or the nervous system). Additionally, the response may either be localized to a specific organ (depending on the metabolic needs of a particular tissue, as during strenuous exercise), or systemic (seen throughout the entire systemic circulation). Factors that result in vasodilation are termed vasodilators.


Vasodilation directly affects the relationship between mean arterial pressure, cardiac output and total peripheral resistance (TPR). Mathematically, cardiac output (blood flow measured in volume per unit time) is computed by multiplying the heart rate (in beats per minute) and the stroke volume (the volume of blood ejected during ventricular systole). TPR depends on several factors including the length of the vessel, the viscosity of blood (determined by hematocrit) and the diameter of the blood vessel. The latter is the most important variable in determining resistance, with the TPR changing by the fourth power of the radius. An increase in either of these physiological components (cardiac output or TPR) cause a rise in the mean arterial pressure. Vasodilation works to decrease TPR and blood pressure through relaxation of smooth muscle cells in the tunica media layer of large arteries and smaller arterioles.[2]

Vasodilation occurs in superficial blood vessels of warm-blooded animals when their ambient environment is hot; this process diverts the flow of heated blood to the skin of the animal, where heat can be more easily released into the atmosphere. The opposite physiological process is vasoconstriction. These processes are naturally modulated by local paracrine agents from endothelial cells (e.g nitric oxide, bradykinin, potassium ions and adenosine), as well as an organism's Autonomic Nervous System and adrenal glands, both of which secrete catecholamines such as norepinephrine and epinephrine, respectively

Examples and individual mechanisms

Vasodilation is the result of relaxation in smooth muscle surrounding the blood vessels. This relaxation, in turn, relies on removing the stimulus for contraction, which depends on intracellular calcium ion concentrations and, consequently, phosphorylation of the light chain of the contractile protein myosin. Thus, vasodilation mainly works either by lowering intracellular calcium concentration or the dephosphorylation of myosin. This includes stimulation of myosin light chain phosphatase and induction of calcium symporters and antiporters that pump calcium ions out of the intracellular compartment. This is accomplished through reuptake of ions into the sarcoplasmic reticulum via exchangers and expulsion across the plasma membrane.[3] There are three main intracellular stimuli that can result in the vasodilation of blood vessels. The specific mechanism to accomplish these effects vary from vasodilator to vasodilator.

Class Description Example
Hyperpolarization mediated (Calcium channel blocker) Changes in the resting membrane potential of the cell affects the level of intracellular calcium through modulation of voltage sensitive calcium channels in the plasma membrane. adenosine
cAMP mediated Adrenergic stimulation results in elevated levels of cAMP and protein kinase A, which results in increasing calcium removal from the cytoplasm prostacyclin
cGMP mediated (Nitrovasodilator) Through stimulation of protein kinase G nitric oxide

PDE5 inhibitors and potassium channel openers can also have similar results.

Compounds that mediate the above mechanisms may be grouped as endogenous and exogenous.


Vasodilators [4] Receptor
(↑ = opens. ↓ = closes) [4]
On vascular smooth muscle cells if not otherwise specified
(↑ = increases. ↓ = decreases) [4]
EDHF  ? hyperpolarization --> ↓VDCC --> ↓intracellular Ca2+
depolarization Voltage-gated K+ channel
interstitial K+ directly
nitric oxide NO receptor on smooth muscle cGMP --> ↑PKG activity -->
  • phosphorylation of MLCK --> ↓MLCK activity --> dephosphorylation of MLC
  • SERCA --> ↓intracellular Ca2+
NO receptor on endothelium Endothelin synthesis [5]
Noradrenaline β-2 adrenergic receptor Gs activity --> ↑AC activity --> ↑cAMP --> ↑PKA activity --> phosphorylation of MLCK --> ↓MLCK activity --> dephosphorylation of MLC
histamine Histamine H1 receptor
prostacyclin IP receptor
Prostaglandin D2 DP receptor
Prostaglandin E2 EP receptor
VIP VIP receptor Gs activity --> ↑AC activity --> ↑cAMP --> ↑PKA activity -->
(extracellular) adenosine A1, A2a and A2b adenosine receptors ATP-sensitive K+ channel --> hyperpolarization --> close VDCC --> ↓intracellular Ca2+
  • (extracellular) ATP
  • (extracellular) ADP
P2Y receptor activate Gq --> ↑PLC activity --> ↑intracellular Ca2+ --> ↑NOS activity --> ↑NO --> (see nitric oxide)
L-Arginine imidazoline and α-2 receptor? Gi --> ↓cAMP --> activation of Na+/K+-ATPase[6] --> ↓intracellular Na+ --> ↑Na+/Ca2+ exchanger activity --> ↓intracellular Ca2+
Bradykinin Bradykinin receptor
Substance P
Niacin (as nicotinic acid only)
Platelet activating factor (PAF)
CO2 - interstitial pH --> ?[7]
(probably) interstitial lactic acid -
muscle work -
Various receptors on endothelium Endothelin synthesis [5]

Therapeutic uses

Vasodilators are used to treat conditions such as hypertension, where the patient has an abnormally high blood pressure, as well as angina and congestive heart failure, where maintaining a lower blood pressure reduces the patient's risk of developing other cardiac problems.[2] Flushing may be a physiological response to vasodilators. Viagra, a phosphodiesterase inhibitor, works to increase blood flow in the penis through vasodilation. It may also be used to treat pulmonary arterial hypertension (PAH).


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de:Vasodilatation es:Vasodilatación fr:Vasodilatateur hr:Vazodilatatori nl:Vasodilatatie ja:血管拡張薬 no:Vasodilator pl:Wazodilatacja pt:Vasodilatação ru:Вазодилатация sr:Вазодилатација sv:Vasodilation tr:Vazodilatör uk:Судинорозширювальні речовини

  1. vasodilation at Dorland's Medical Dictionary
  2. 2.0 2.1 CVPharmacology
  3. American Physiological Society
  4. 4.0 4.1 4.2 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
  5. 5.0 5.1 5.2 5.3 5.4 5.5 5.6 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. Regulation of Na+-K+-ATPase by cAMP-dependent protein kinase anchored on membrane via its anchoring protein Kinji Kurihara, Nobuo Nakanishi, and Takao Ueha. Departments of 1 Oral Physiology and 2 Biochemistry, School of Dentistry, Meikai University, Sakado, Saitama 350-0283, Japan
  7. Modin A, Björne H, Herulf M, Alving K, Weitzberg E, Lundberg JO (2001). "Nitrite-derived nitric oxide: a possible mediator of 'acidic-metabolic' vasodilation". Acta Physiol. Scand. 171 (1): 9–16. doi:10.1046/j.1365-201x.2001.171001009.x. PMID 11350258.