adenosine adenosine adenosine (symbol a) is an organic compound that occurs widely in nature in the form of diverse derivatives. the molecule consists of an adenine attached to a ribose via a β-n9-glycosidic bond. adenosine is one of the four nucleoside building blocks of rna (and its derivative deoxyadenosine is a building block of dna), which are essential for all life. its derivatives include the energy carriers adenosine mono-, di-, and triphosphate, also known as amp/adp/atp. cyclic adenosine monophosphate (camp) is pervasive in signal transduction. adenosine is used as an intravenous medication for some cardiac arrhythmias. adenosineclinical datatrade namesadenocard; adenocor; adenic; adenoco; adeno-jec; adenoscan; adenosin; adrekar; krenosinother namessr-96225 (developmental code name)ahfs/drugs.commonographpregnancycategory c (adenosine may be safe to the fetus in pregnant women) routes ofadministrationintravenousatc codec01eb10 (who) legal statuslegal status in general: ℞ (prescription only) pharmacokinetic databioavailabilityrapidly cleared from circulation via cellular uptakeprotein bindingnometabolismrapidly converted to inosine and adenosine monophosphateelimination half-lifecleared plasma <30 seconds; half-life <10 secondsexcretioncan leave cell intact or can be degraded to hypoxanthine, xanthine, and ultimately uric acididentifiers iupac name (2r,3r,4s,5r)-2-(6-amino-9h-purin-9-yl)-5-(hydroxymethyl)oxolane-3,4-diol cas number58-61-7 ypubchem cid60961iuphar/bps2844drugbankdb00640 ychemspider54923 yuniik72t3fs567keggc00212 ychebichebi:16335 ychemblchembl477 ncomptox dashboard (epa)dtxsid1022558 echa infocard100.000.354 chemical and physical dataformulac10h13n5o4molar mass267.245 g·mol−13d model (jsmol)interactive image smiles n2c1c(ncnc1n(c2)3o((o)3o)co)n inchi inchi=1s/c10h13n5o4/c11-8-5-9(13-2-12-8)15(3-14-5)10-7(18)6(17)4(1-16)19-10/h2-4,6-7,10,16-18h,1h2,(h2,11,12,13)/t4-,6-,7-,10-/m1/s1 ykey:oirdtqyftabqoq-kqynxxcusa-n y ny (what is this?) (verify) adenosyl (abbreviated ado or 5'-dado) is the chemical group formed by removal of the 5′-hydroxy (oh) group. it is found in adenosylcobalamin (an active form of vitamin b12) and as a radical in radical sam enzymes. medical uses supraventricular tachycardia in individuals with supraventricular tachycardia (svt), adenosine is used to help identify and convert 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) and av nodal reentrant tachycardia (avnrt). in addition, atrial tachycardia can sometimes be terminated with adenosine. fast rhythms of the heart that are confined to the atria (e.g., atrial fibrillation and 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 is temporarily slowed with adenosine in such cases. 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 disconcerting to a normally conscious patient, and is associated with angina-like sensations in the chest. nuclear stress test adenosine is used as an adjunct to thallium (ti 201) or technetium (tc99m) myocardial perfusion scintigraphy (nuclear stress test) in patients unable to undergo adequate stress testing with exercise. dosage when given for the evaluation or treatment of a supraventricular tachycardia (svt), the initial dose is 6 mg to 12 mg, depending on standing orders or provider preference, given as a rapid parenteral infusion. due to adenosine's extremely short half-life, the iv line is started as proximal (near) to the heart as possible, such as the antecubital fossa. the iv push is often followed with a flush of 10–20 ml of normal saline. if this has no effect (i.e., no evidence of transient av block), a dose of 12 mg can be given 1–2 minutes after the first dose. 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. the recommended dose may be increased in patients on theophylline since methylxanthines prevent binding of adenosine at receptor sites. the dose is often decreased in patients on dipyridamole (persantine) and diazepam (valium) because adenosine potentiates the effects of these drugs. the recommended dose is also reduced by half in patients presenting congestive heart failure, myocardial infarction, shock, hypoxia, and/or chronic liver disease or chronic kidney disease, and in elderly patients. drug interactions dipyridamole potentiates the action of adenosine, requiring the use of lower doses. caffeine's principal mode of action is as an antagonist of adenosine receptors in the brain. methylxanthines (e.g. caffeine found in coffee, theophylline found in tea, or theobromine found in chocolate) have a purine structure and bind to some of the same receptors as adenosine. methylxanthines act as competitive antagonists of adenosine and can blunt its pharmacological effects. individuals taking large quantities of methylxanthines may require increased doses of adenosine. caffeine acts by blocking binding of adenosine to the adenosine a1 receptor, which enhances release of the neurotransmitter acetylcholine. caffeine also increases cyclic amp levels through nonselective inhibition of phosphodiesterase. "caffeine has a three-dimensional structure similar to that of adenosine," which allows it to bind and block its receptors. contraindications common contraindications for adenosine include asthma, traditionally considered an absolute contraindication. this is being contended and it is now considered a relative contraindication (however, selective adenosine antagonists are being investigated for use in treatment of asthma) pharmacological effects adenosine is an endogenous purine nucleoside that modulates many physiological processes. cellular signaling by adenosine occurs through four known adenosine receptor subtypes (a1, a2a, a2b, and a3). 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 regard 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. enzymatic production of adenosine can be anti-inflammatory or immunosuppressive. adenosine receptors all adenosine receptor subtypes (a1, a2a, a2b, and a3) are g-protein-coupled receptors. the four receptor subtypes are further classified based on their ability to either stimulate or inhibit adenylate cyclase activity. the a1 receptors couple to gi/o and decreases camp levels, while the a2 adenosine receptors couple to gs, which stimulates adenylate cyclase activity. in addition, a1 receptors couple to go, which has been reported to mediate adenosine inhibition of ca2+ conductance, whereas a2b and a3 receptors also couple to gq and stimulate phospholipase activity. researchers at cornell university have recently shown adenosine receptors to be key in opening the blood-brain barrier (bbb). mice dosed with adenosine have shown increased transport across the bbb of amyloid plaque antibodies and prodrugs associated with parkinson's disease, alzheimer's, multiple sclerosis, and cancers of the central nervous system. ghrelin/growth hormone secretagogue receptor adenosine is an endogenous agonist of the ghrelin/growth hormone secretagogue receptor. however, while it is able to increase appetite, unlike other agonists of this receptor, adenosine is unable to induce the secretion of growth hormone and increase its plasma levels. mechanism of action when it is administered intravenously, adenosine causes transient heart block in the atrioventricular (av) node. this is mediated via the a1 receptor, inhibiting adenylyl cyclase, reducing camp and so causing cell hyperpolarization by increasing k+ efflux via inward rectifier k+ channels, subsequently inhibiting ca2+ current. it also causes endothelial-dependent relaxation of smooth muscle as is found inside the artery walls. this causes dilation of the "normal" segments of arteries, i.e. 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. the administration of adenosine also reduces blood flow to coronary arteries past the occlusion. other coronary arteries dilate when adenosine is administered while the segment past the occlusion is already maximally dilated, which is a process called coronary steal. this leads to less blood reaching the ischemic tissue, which in turn produces the characteristic chest pain. metabolism adenosine used as a second messenger can be the result of de novo purine biosynthesis via adenosine monophosphate (amp), though it is possible other pathways exist. when adenosine enters the circulation, it is broken down by adenosine deaminase, which is present in red blood cells and the vessel wall. dipyridamole, an inhibitor of adenosine nucleoside transporter, allows adenosine to accumulate in the blood stream. this causes an increase in coronary vasodilatation. adenosine deaminase deficiency is a known cause of immunodeficiency. research viruses