Chemical formula: C₁₀H₁₃N₅O₄ Molecular mass: 267.241 g/mol PubChem compound: 60961
Adenosine is a potent vasodilator in most vascular beds, except in renal afferent arterioles and hepatic veins where it produces vasoconstriction. Adenosine exerts its pharmacological effects through activation of purine receptors (cell-surface A1 and A2 adenosine receptors). Although the exact mechanism by which adenosine receptor activation relaxes vascular smooth muscle is not known, there is evidence to support both inhibition of the slow inward calcium current reducing calcium uptake, and activation of adenylate cyclase through A2 receptors in smooth muscle cells. Adenosine may reduce vascular tone by modulating sympathetic neurotransmission. The intracellular uptake of adenosine is mediated by a specific transmembrane nucleoside transport system. Once inside the cell, adenosine is rapidly phosphorylated by adenosine kinase to adenosine monophosphate, or deaminated by adenosine deaminase to inosine. These intracellular metabolites of adenosine are not vasoactive.
Intracoronary Doppler flow catheter studies have demonstrated that intravenous adenosine at 140 µg/kg/min produces maximum coronary hyperaemia (relative to intracoronary papaverine) in approximately 90% of cases within 2–3 minutes of the onset of the infusion. Coronary blood flow velocity returns to basal levels within 1–2 minutes of discontinuing the adenosine infusion.
The increase in blood flow caused by adenosine in normal coronary arteries is significantly more than that in stenotic arteries. Adenosine redirects coronary blood flow from the endocardium to the epicardium and may reduce collateral coronary blood flow thereby inducing regional ischaemia.
Continuous infusion of adenosine in man has been shown to produce a mild dose-dependent fall in mean arterial pressure and a dose-related positive chronotropic effect, most likely caused by sympathetic stimulation. The onset of this reflex increase in heart rate occurs later than the negative chronotropic/dromotropic effect. This differential effect is mostly observed after bolus injection thus explaining the potential use of adenosine as a treatment for supraventricular arrhythmias when administered as a bolus or as a coronary vasodilator when administered as an infusion.
Although adenosine affects cardiac conduction, it has been safely and effectively administered in the presence of other cardioactive or vasoactive drugs such as beta-adrenergic blocking agents, calcium channel antagonists, nitrates, ACE inhibitors, diuretics, digitalis or anti-arrhythmics.
It is impossible to study adenosine in classical pharmacokinetic studies. It is present in various forms in all the cells of the body where it plays an important role in energy production and utilisation systems. An efficient salvage and recycling system exists in the body, primarily in erythrocytes and blood vessel endothelial cells.
The half-life in vitro is estimated to be less than 10 seconds. The in vivo half-life may be even shorter.
Since neither the kidney nor the liver are involved in the degradation of exogenous adenosine, the efficacy of adenosine should be unaffected by hepatic or renal insufficiency.
Because adenosine is naturally present in all living cells, studies in animals to evaluate the carcinogenic potential of Adenoscan (adenosine) have not been performed.
No controlled reproductive studies were conducted in animals with adenosine.
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