Vasodilation

This article needs more primary sources. Please review the contents of the article and add the appropriate references if you can. Unsourced or poorly sourced material may be challenged and removed. Find sources: "Vasodilation" – news · newspapers · books · scholar · JSTOR (March 2021)

Vasodilation, also known as vasorelaxation, is the widening of blood vessels.^[1] It results from relaxation of smooth muscle cells within the vessel walls, in particular in the large veins, large arteries, and smaller arterioles.^[2] Blood vessel walls are composed of endothelial tissue and a basal membrane lining the lumen of the vessel, concentric smooth muscle layers on top of endothelial tissue, and an adventitia over the smooth muscle layers.^[3] Relaxation of the smooth muscle layer allows the blood vessel to dilate, as it is held in a semi-constricted state by sympathetic nervous system activity.^[2] Vasodilation is the opposite of vasoconstriction, which is the narrowing of blood vessels.

When blood vessels

Endogenous substances and drugs that cause vasodilation are termed vasodilators. Many of these substances are neurotransmitters released by perivascular nerves of the autonomic nervous system^[6] Baroreceptors sense blood pressure and allow adaptation via the mechanisms of vasoconstriction or vasodilation to maintain homeostasis.^[2]

Function

The primary function of vasodilation is to increase blood flow in the body to tissues that need it most. This is often in response to a localized

Vasodilation plays a major role in immune system function. Wider blood vessels allow more blood containing immune cells and proteins to reach the infection site. Vasodilation occurs as part of the process of inflammation, which is caused by several factors including presence of a pathogen, injury to tissues or blood vessels, and immune complexes.^[7] In severe cases, inflammation can lead to sepsis or distributive shock.^[11] Vasodilation is also a major component of anaphylaxis.^[12]

Inflammation causes not only vasodilation but also causes increased

Vascular resistance depends on several factors, including the length of the vessel, the viscosity of blood (determined by hematocrit) and the diameter of the blood vessel.^[18] The latter is the most important variable in determining resistance, with the vascular resistance changing by the fourth power of the radius.^[2] An increase in either of these physiological components (cardiac output or vascular resistance) causes a rise in MAP. Arterioles create the most vascular resistance of any blood vessel type, as they are very narrow and possess concentric layers of smooth muscle unlike venules and capillaries.^[2]

Vasodilation occurs in superficial blood vessels of

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

Compounds that mediate the above mechanisms may be grouped as

Causes

Endogenous

The vasodilating action of activation of

As referenced in the explanation of smooth muscle physiology, smooth muscle within the tunica media is innervated by the autonomic nervous system. The autonomic nervous system (ANS) controls essential involuntary body functions and originates as nerves leaving the brain stem or spinal cord; it contains both sensor and motor nerves.^[2] The two divisions of the ANS, the sympathetic nervous system (SNS) and the parasympathetic nervous system (PSNS), impact blood vessels differently.^[2] Traditionally we understand that these two divisions work against each other, the SNS producing "fight or flight" and the PSNS producing "rest and digest", but in the case of vascular innervation this line becomes blurred^[6] ANS nerves do not directly innervate the vasculature via synapses with muscle cells; instead, they release neurotransmitters that reach target cells and effect smooth muscle contraction or relaxation.^[6] Physical characteristics of the SNS and PSNS cause the SNS to have a prolonged, systemic impact on blood vessels, while the PSNS causes short-lived, localized change.^[2] SNS stimulation causes a base level of vasoconstriction often referred to as basal neural tone, maintaining blood pressure.^[2] Often vasodilation is simply the result of insufficient neurotransmitter to maintain basal neural tone, without the presence of a compound directly causing vasodilation.^[2]

Neurotransmitters can act by binding directly to smooth muscle cells or by binding to endothelial cells mediating the effects of the neurotransmitter.^[6] Below is a table summarizing major neurotransmitters involved in regulation of the vasculature.

Also worthy of mention when discussing neural control of vasodilation is the renin-angiotensin-aldosterone system, or RAAS.^[2] The kidneys retain water by reabsorbing sodium ions, or eliminate water by eliminating sodium ions.^[29] Sympathetic nervous system activity, reduced blood volume or reduced arterial pressure trigger β-adrenergic receptors in select kidney cells^[2] to release renin, which converts facilitates formation of angiotensin II from its substrate angiotensin.^[29] Angiotensin II triggers adrenal glands to secrete aldosterone, a potent vasoconstrictor.^[29]

Cold-induced vasodilation (CIVD) occurs after cold exposure, possibly to reduce the risk of injury. It can take place in several locations in the human body but is observed most often in the extremities. The fingers are especially common because they are exposed most often.^[citation needed]

When the fingers are exposed to cold,

A new phase of vasoconstriction follows the vasodilation, after which the process repeats itself. This is called the Hunting reaction. Experiments have shown that three other vascular responses to immersion of the finger in cold water are possible: a continuous state of vasoconstriction; slow, steady, and continuous rewarming; and a proportional control form in which the blood vessel diameter remains constant after an initial phase of vasoconstriction. However, the vast majority of responses can be classified as the Hunting reaction.^[30]

Miscellaneous

This section needs more primary sources. Please review the contents of the section and add the appropriate references if you can. Unsourced or poorly sourced material may be challenged and removed. Find sources: "Vasodilation" – news · newspapers · books · scholar · JSTOR (March 2022)

• Other suggested vasodilators or vasodilating factors include:
  • absence of high levels of environmental noise^[31]
  • arrhythmic^[32]
  • vasoconstricting effect of adrenaline)^[33]
  • atrial natriuretic peptide (ANP) - a weak vasodilator^[34]
  • ethanol (alcohol) causes immediate vasodilation followed by increase in blood pressure^[35]
  • nitric oxide inducers
    • l-arginine (a key amino acid)^[36]
    • citrulline (causes increased levels of L-arginine in the body)^[37]
    • glyceryl trinitrate (commonly known as nitroglycerin)^[38]
    • isosorbide mononitrate and isosorbide dinitrate^[39]
    • pentaerythritol tetranitrate (PETN)^[40]
    • sodium nitroprusside^[41]
    • PDE5 inhibitors: these agents indirectly increase the effects of nitric oxide^[42]
      • sildenafil (Viagra)
      • tadalafil (Cialis)
      • vardenafil (Levitra)
  • tetrahydrocannabinol (THC), the principal psychoactive constituent of cannabis^[43]
  • theobromine, the principal alkaloid found in Theobroma cacao, specifically in cocoa solids (which is found in chocolate, especially dark chocolate)^[44]
  • minoxidil^[45]
  • papaverine an alkaloid found in the opium poppy papaver somniferum^[46]
  • estrogen^[47]

Treatment

Direct vasodilation drugs

These drugs can keep vessels staying opened or help vessels refrain from being narrowed.^[48]

• Angiotensin II receptor blockers
• ACE inhibitors
• Calcium channel blockers

Alpha-2A adrenergic receptor agonists

Drugs that appear to work by activating the α_2A receptors in the brain thereby decreasing sympathetic nervous system activity.^[49][48]

• methyldopa

According to American Heart Association, Alpha-methyldopa may cause Orthostatic syncope as it exerts a greater blood pressure lowering effect when one is standing upright which may lead to feeling weak or fainting if the blood pressure has been lowered too far. Methyldopa's prominent side effects include drowsiness or sluggishness, dryness of the mouth, fever or anemia. Additionally to these, male patients may experience impotence.^[48]

• clonidine hydrochloride
• guanabenz acetate
• guanfacine hydrochloride

Clonidine, guanabenz or guanfacine may give rise to severe dryness of the mouth, constipation or drowsiness. Abrupt cessation taking may raise blood pressure quickly to dangerously high levels.^[48]

Blood vessel muscle relaxants

Directly relax the muscle in the walls of the blood vessels (especially the arterioles), allowing the vessel to dilate (widen).^[48]

• hydralazine
• minoxidil

Hydralazine may cause headaches, swelling around the eyes, heart palpitations or aches and pains in the joints. In clinical setting, hydralazine is not usually used alone.^[48]

Minoxidil is a potent direct vasodilator used only in resistant severe high blood pressure or when kidney failure is present. Noted adverse effects comprise fluid retention (marked weight gain) and excessive hair growth.^[48]

Therapeutic applications

Vasodilators are used to treat conditions such as

• Arteriolar vasodilator
• Nitrophorin
• Vasodilatory shock

References

Scholia has a topic profile for Vasodilation.