Vasodilator: Wikis

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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.


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 i ! 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 [2] Receptor
(↑ = opens. ↓ = closes) [2]
(↑ = increases. ↓ = decreases) [2]
EDHF  ? hyperpolarization --> ↓VDCC --> ↓intracellular Ca2+
depolarization Voltage-gated K+ channel
interstitial K+ directly
nitric oxide NO receptor cGMP --> ↑PKG activity -->
  • phosphorylation of MLCK --> ↓MLCK activity --> dephosphorylation of MLC
  • SERCA --> ↓intracellular Ca2+
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[3] --> ↓intracellular Na+ --> ↑Na+/Ca2+ exchanger activity --> ↓intracellular Ca2+
Bradykinin Bradykinin receptor
Substance P
Niacin (nicotinic acid)
Platelet activating factor (PAF)
CO2 - interstitial pH --> ?[4]
(probably) interstitial lactic acid -
muscle work -

Exogenous vasodilators

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.[5] 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).


  1. ^ vasodilation at Dorland's Medical Dictionary
  2. ^ 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
  3. ^ 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
  4. ^ 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.  
  5. ^ CVPharmacology

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