Endogenous signalling nucleoside acting at four GPCR subtypes: A1 (cardiac slowing, inhibition of NE release), A2A (vasodilation, wakefulness suppression — caffeine's principal target), A2B, A3. Accumulates with neural activity and is the presumed somnogen driving sleep pressure. Extremely short plasma t½ (seconds) — deaminated to inosine by adenosine deaminase.
Half-Life (t½)
IV: 0.0028h
Dosing Guidelines
IV: Typical 6 mg (Range: 6–6 mg)
Target Organ Systems
cardiovascular
Interactions
Caffeine (caution): Caffeine is a non-selective A1/A2A antagonist — reduces endogenous adenosine effects and blunts IV adenosine's clinical potency (hold caffeine ≥24 h before stress testing).
Dipyridamole (major): Dipyridamole blocks ENT1-mediated cellular re-uptake of adenosine, raising extracellular levels severalfold and profoundly amplifying SA/AV-node slowing, vasodilation, and risk of bronchospasm from exogenous IV adenosine — reduce IV adenosine dose or choose an alternate stress agent. [Meester 1998]
PEAK ATP (synergistic): Adenosine is the terminal dephosphorylation product — extracellular signalling convergence.