Vasodilation refers to the widening of blood vessels resulting from relaxation of smooth muscle cells within the vessel walls, particularly in the large arteries, arterioles and 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) or extrinsic (due to hormones or the nervous system), as well organ specific or systemic. Factors that result in vasodilation are simply termed vasodilators.

Function

Vasodilation directly affects the relationship between mean arterial pressure and cardiac output and total peripheral resistance (TPR). Mathematically, cardiac output is computed by multiplying the heart rate (in beats/minute) and the stroke volume (the volume of blood ejected during 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. An increase in either of these physiological components (cardiac output or TPR) cause a rise in the mean arterial pressure. Vasodilators work to decrease TPR and blood pressure through relaxation of smooth muscle cells in the tunica media layer of large arteries and smaller arterioles.^[1]

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 a result of relaxation in smooth muscle surrounding the blood vessels. This relaxation, in turn, relies on removing the stimulus for contraction, which depends predominately on intracellular calcium ion concentrations and phosphorylation of myosin light chain (MLC). Thus, vasodilation mainly works either by lowering intracellular calcium concentration or dephosphorylation of MLC. 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. ^[2] There are three main stimuli that can result in the vasodilation of blood vessels, the specific mechanisms to accomplish these effects varying from vasodilator to vasodilator.

1. Hyperpolarization-Mediated: 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.
2. cAMP-Mediated: Adrenergic stimulation results in elevated levels of cAMP and protein kinase A, which results in elevating calcium removal from the cytoplasm
3. cGMP-Mediated: Endothelium-derived relaxing factor (also known as nitric oxide), a potent vasodilator, operates through this mechanism through stimulation of protein kinase G.

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

Endogenous

Exogenous vasodilators

• Absence of high levels of environmental noise
• Absence of high levels of illumination
• Adenocard - Adenosine agonist, primarily used as an anti-arrhythmic.
• Alpha blockers (block the vasoconstricting effect of adrenaline).
• Amyl nitrite and other nitrites are often used recreationally as a vasodilator, causing lightheadedness and a euphoric feeling.
• Atrial natriuretic peptide (ANP) - a weak vasodilator.
• Ethanol
• Histamine-inducers
  • Complement proteins C3a, C4a and C5a work by triggering histamine release from mast cells and basophil granulocytes.
• Nitric oxide inducers
  • Glyceryl trinitrate (commonly known as Nitroglycerin)
  • Isosorbide mononitrate & Isosorbide dinitrate
  • Pentaerythritol Tetranitrate (PETN)
  • Sodium nitroprusside
  • PDE5 inhibitors: these agents indirectly increase the effects of nitric oxide
    • Sildenafil (Viagra)
    • Tadalafil
    • Vardenafil
• Tetrahydrocannabinol (THC) - the major active chemical in marijuana. Its mild vasodilating effects redden the eyes of cannabis smokers.
• Theobromine.
• Papaverine an alkaloid found in the opium poppy papaver somniferum

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.^[6] Flushing may be a physiological response to vasodilators.

References

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