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A vasodilator is a drug or chemical that relaxes the smooth muscle in blood vessels, which causes them to dilate. Dilation of arterial blood vessels (mainly arterioles) lead to a decrease in blood pressure.

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 the organism's Autonomic Nervous System and adrenal glands, both of which secrete catecholamines such as norepinephrine and epinephrine, respectively.

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 by 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 retuptake of ions into the sarcoplasmic reticulum via exchangers and expulsion across the plasma membrane. ^[2] The specific mechanisms to accomplish these effects varies from vasodilator to vasodilator.

These may be grouped as endogenous and

• 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

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 a maintaining a lower blood pressure reduces the patient's risk of developing other cardiac problems.^[7] Flushing may be a physiological response to vasodilators.

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