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Caffeine, an unspecific antagonist of adenosine receptors, is commonly used to treat the apnea of prematurity. We have defined the effects of caffeine on the carotid body (CB) chemoreceptors, the main peripheral controllers of breathing, and identified the adenosine receptors involved. Caffeine inhibited basal (IC₅₀, 210 µm) and low intensity (PO₂ ≈ 66 mm Hg/30 mm K⁺) stimulation‐induced release of catecholamines from chemoreceptor cells in intact preparations of rat CB in vitro. Opposite to caffeine, 5′‐(N‐ethylcarboxamido)adenosine (NECA; an A₂ agonist) augmented basal and low‐intensity hypoxia‐induced release. 2‐p‐(2‐Carboxyethyl)phenethyl‐amino‐5′‐N‐ethylcaboxamido‐adenosine hydrochloride (CGS21680), 2‐hexynyl‐NECA (HE‐NECA) and SCH58621 (A_2A receptors agents) neither affected catecholamine release nor altered the caffeine effects. The 8‐cycle‐1,3‐dipropylxanthine …