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  • endogenous compound found in virtually all cell types
  • nucleoside: adenine + D-ribose
  • formed from AMP or S-adenosylhomocysteine. Can be formed either intracellularly or extracellularly. Degradation requires uptake by cells as it involves intracellular enzymes. Transport system is inhibited by dipyridamole


  • 3 types of receptors. A1 and A2 receptors are subtypes of P1 class of receptors
  • A1 or A2 agonist-receptor complex is responsible for inhibition or stimulation of adenylate cyclase and a decrease or increase in intracellular cAMP respectively.
  • adenosine also has actions which are not mediated via cAMP
  • both cAMP mediated effects and other actions appear to be mediated by G proteins
  • A1 and A2 receptors blocked by methylxanthines such as theophylline
  • A3 receptor has recently been characterized. It is resistant to blockade by methylxanthines but may be stimulated by both A1 and A2 agonists

Cardiac electrophysiological effects

  • mostly mediated by A1 receptor
  • depression of sinus node automaticity and AVN conduction. Associated with an increase in PR and AV intervals but not in HV interval, suggesting a site of action proximal to bundle of His. Mediated by:
  • activation of a specific outward K current which is independent of adenylate cyclase. Results in shortening of the atrial action potential, hyperpolarisation of the SAN cells and depression of the amplitude, duration and rate of rise of action potential in AVN cells.
  • attenuation of effects of catecholamines by inhibiting adenylate cyclase stimulation of the inward calcium current in atrial and ventricular myocytes. Greater inhibition of this current occurs after previous stimulation by beta agonists
  • stimulation of presynaptic adrenergic receptors on adrenergic nerves which decreases the amount of norepinephrine released for any given level of sympathetic stimulation

Haemodynamic effects

  • result of interplay between direct effects and indirect effects mediated through alterations in autonomic nervous system tone
  • potent vasodilator with dose-related decrease in peripheral vascular resistance. Affects almost all vascular beds. May be a direct result of A2 receptor activation or may involve release of endothelium-derived relaxing factor or prostaglandin. Has little effect on CVP, suggesting that it has little effect on capacitance vessels
  • decrease in peripheral vascular resistance results in increased cardiac output. Non-hypotensive doses can cause a rise in cardiac index of 50% and an improvement in early ventricular filling dynamics. Increase in cardiac output may cause a rise in systolic and mean PAP despite a decrease in pulmonary vascular resistance
  • adenosine-induced decreases in BP may cause an increase in heart rate through activation of baroreflexes. Response is less than that seen with other vasodilators, partly as a result of direct negative chronotropic effects
  • directly stimulates afferent nerves, including chemoreceptors to increase sympathetic tone
  • negative chronotropic effects in combination with potent vasodilatation may cause profound hypotension during anaesthesia or in patients with intravascular volume depletion
  • coronary vasodilator (via A2 receptor). May play a role in coronary autoregulation with increased adenosine concentrations resulting from increased ATP utilization. Predominantly affects small coronary arterioles. Exogenously administered adenosine may result in coronary steal
  • in renal circulation produces A2 receptor mediated vasodilatation of postglomerular efferent arterioles and A1 receptor-mediated constriction of afferent arterioles. Latter results in a decrease in GFR, RBF, filtration fraction and urine flow
  • in pulmonary circulation causes vasodilatation. Can result in inhibition of hypoxic pulmonary vasoconstriction and increased pulmonary shunt

Myocardial protection

  • appears to be an endogenous protective agent during ischaemia and reperfusion injury
  • has direct actions to attenuate ischaemia, reduce infarction, and enhance recovery of reperfused myocardium although when administered exogenously may cause myocardial ischaemia. Difference in effect relates to site of delivery of adenosine. In patients with a steal-prone anatomy adenosine will be delivered predominantly to collaterals while in patients with endogenously produced adenosine secondary to ischaemia the adenosine concentration will be highest in the ischaemic region

Drug interactions

  • dipyridamole potentiates action by inhibiting uptake
  • methylxanthines are competitive antagonists and may necessitate larger doses
  • can be safely administered to patients taking digoxin, quinidine, beta blockers, calcium blockers, ACE inhibitors

Adverse effects

  • occur in approx 20% but are brief (<1 min)
  • include:
    • facial flushing
    • SOB
    • chest tightness
    • asystole


  • not recommended in patients with sick sinus syndrome due to possibility of prolonged heart block
  • bronchospasm

© Charles Gomersall December 1999


©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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