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Adenosine chemical structure

(2R,3R,4R,5R)-2-(6-aminopurin-9-yl)- 5-(hydroxymethyl)oxolane-3,4-diol
IUPAC name
CAS number
ATC code


Chemical formula {{{chemical_formula}}}
Molecular weight 267.242 g/mol
Bioavailability Rapidly cleared from circulation via cellular uptake
Metabolism Rapidly converted to inosine and adenosine monophosphate
Elimination half-life cleared plasma <30 seconds - half life <10 seconds
Excretion can leave cell intact or can be degraded to hypoxanthine, xanthine, and ultimately uric acid
Pregnancy category C
Legal status Australia - Legal; UK - Legal; US - Rx only
Routes of administration IV or injection

Adenosine is a nucleoside comprised of adenine attached to a ribose (ribofuranose) moiety via a β-N9-glycosidic bond.

Adenosine plays an important role in biochemical processes, such as energy transfer - as adenosine triphosphate (ATP) and adenosine diphosphate (ADP) - as well as in signal transduction as cyclic adenosine monophosphate, cAMP. It is also an inhibitory neurotransmitter, believed to play a role in promoting sleep and suppressing arousal, with levels increasing with each hour an organism is awake.

Pharmacological effects

Adenosine is an endogenous purine nucleoside that modulates many physiologic processes. Cellular signaling by adenosine occurs through four known adenosine receptor subtypes (A1, A2A, A2B, and A3), all of which are seven transmembrane spanning G-protein coupled receptors. These four receptor subtypes are further classified based on their ability to either stimulate or inhibit adenylate cyclase activity. The A2A and A2B receptors couple to Gάs and mediate the stimulation of adenylate cyclase, while the A1 and A3 adenosine receptors couple to Gάi which inhibits adenylate cyclase activity. Additionally, A1 receptors couple to Gάo, which has been reported to mediate adenosine inhibition of Ca2+ conductance, whereas A2B and A3 receptors also couple to Gάq and stimulate phospholipase activity. Extracellular adenosine concentrations from normal cells are approximately 300 nM; however, in response to cellular damage (e.g. in inflammatory or ischemic tissue), these concentrations are quickly elevated (600-1,200 nM). Thus, in regards to stress or injury, the function of adenosine is primarily that of cytoprotection preventing tissue damage during instances of hypoxia, ischemia, and seizure activity. Activation of A2A receptors produces a constellation of responses that in general can be classified as anti-inflammatory.

Anti-inflammatory Properties

Adenosine is a potent anti-inflammatory agent, acting at its four G-protein coupled receptors. Topical treatment of adenosine to foot wounds in diabetes mellitus has been shown in lab animals to drastically increase tissue repair and reconstruction. Topical administration of adenosine for use in wound healing deficiencies and diabetes mellitus in humans is currently under clinical investigation.

Action on the heart

When administered intravenously, adenosine causes transient heart block in the AV node. This is mediated via the A1 receptor, inhibiting adenyl cyclase, reducing cAMP and so causing cell hyperpolarisation by increasing outward K flux. It also causes endothelial dependent relaxation of smooth muscle as is found inside the artery walls. This causes dilatation of the "normal" segments of arteries where the endothelium is not separated from the tunica media by atherosclerotic plaque. This feature allows physicians to use adenosine to test for blockages in the coronary arteries, by exaggerating the difference between the normal and abnormal segments.

In individuals suspected of suffering from a supraventricular tachycardia (SVT), adenosine is used to help identify the rhythm. Certain SVTs can be successfully terminated with adenosine. This includes any re-entrant arrhythmias that require the AV node for the re-entry (e.g., AV reentrant tachycardia (AVRT), AV nodal reentrant tachycardia (AVNRT). In addition, atrial tachycardia can sometimes be terminated with adenosine.

Adenosine has an indirect effect on atrial tissue causing a shortening of the refractory period. When administered via a central lumen catheter, adenosine has been shown to initiate atrial fibrillation because of its effect on atrial tissue. In individuals with accessory pathways, the onset of atrial fibrillation can lead to a life threatening ventricular fibrillation.

Fast rhythms of the heart that are confined to the atria (e.g., atrial fibrillation, atrial flutter) or ventricles (e.g., monomorphic ventricular tachycardia) and do not involve the AV node as part of the re-entrant circuit are not typically converted by adenosine, however the ventricular response rate will be temporarily slowed.

Because of the effects of adenosine on AV node-dependent SVTs, adenosine is considered a class V antiarrhythmic agent. When adenosine is used to cardiovert an abnormal rhythm, it is normal for the heart to enter ventricular asystole for a few seconds. This can be very disconcerting to a normally conscious patient, and is associated with very unpleasant sensations in the chest.

Caffeine's principal mode of action is as an antagonist of adenosine receptors in the brain. They are presented here side by side for comparison.

The pharmacological effects of adenosine may be blunted in individuals who are taking large quantities of methylxanthines (e.g., caffeine (found in coffee) and theophylline (found predominantly in tea)).

Caffeine's stimulatory effects are primarily (although not entirely) credited to its inhibition of adenosine by binding to the same receptors. By nature of caffeine's purine structure it binds to some of the same receptors as adenosine, effectively blocking adenosine receptors in the central nervous system. This reduction in adenosine activity leads to increased activity of the neurotransmitters dopamine and glutamate.


When given for the evaluation or treatment of an SVT, the initial dose is 6 mg, given as a fast IV/Intraosseous IO push. Due to adenosine's extremely short half-life, start the IV line as proximal to the heart as possible, such as the antecubital fossa. It is also recommended to follow the IV push with an immediate flush of 5-10ccs of saline. If this has no effect (e.g., no evidence of transient AV block), a 12mg dose can be given 1-2 minutes after the first dose. If the 12mg dose has no effect, a second 12mg dose can be administered 1-2 minutes after the previous dose. Some clinicians may prefer to administer a higher dose (typically 18 mg), rather than repeat a dose that apparently had no effect. When given to dilate the arteries, such as in a "stress test", the dosage is typically 0.14 mg/kg/min, administered for 4 or 6 minutes, depending on the protocol.

Consider increasing the recommended dose in patients on theophylline since methylxanthines prevent binding of adenosine at receptor sites. Consider decreasing the dose in patients on dipyridamole (Persantine) and diazepam (Valium) because adenosine potentiates the effects of these drugs.

Consider decreasing the recommended dose in half in patients who are presenting Congestive Heart Failure, Myocardial Infarction, shock, hypoxia, and/or hepatic or renal insufficiency.

Consider decreasing the recommended dose in half for elderly patients.

Drug Interactions

Beta blockers and dopamine may precipitate toxicity in the patient.


Poison/Drug induced tachycardia, Asthma (relative contraindication), 2nd or 3rd degree heart block, Atrial fibrillation, atrial flutter, Ventricular tachycardia, Sick sinus syndrome, Stokes-Adams Attack, Wolf-Parkinson-White syndrome, bradycardia with Premature Ventricular Contractions (PVCs).

  • WPW- adenosine may be administered if equipment for cardioversion is immediately available as a backup.
  • A-flutter W/rvr - when it first presents with SVT

Side effects

Many individuals experience facial flushing, lightheadedness, diaphoresis, or nausea after administration of adenosine. These symptoms are transitory, usually lasting less than one minute.


When adenosine enters the circulation, it is broken down by adenosine deaminase, which is present in red cells and the vessel wall.

Dipyridamole, an inhibitor of adenosine deaminase, allows adenosine to accumulate in the blood stream. This causes an increase in coronary vasodilatation.

See also

External links

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