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Adenosine and nitric oxide (NO) are important local mediators of vasodilatation. The aim of this study was to elucidate the mechanisms underlying adenosine receptor‐mediated NO release from the endothelium. In studies on freshly excised rat aorta, second‐messenger systems were pharmacologically modulated by appropriate antagonists while a NO‐sensitive electrode was used to measure adenosine‐evoked NO release from the endothelium. We showed that A₁‐mediated NO release requires extracellular Ca²⁺, phospholipase A₂ (PLA₂) and ATP‐sensitive K⁺ (K_ATP) channel activation whereas A_2A‐mediated NO release requires extracellular Ca²⁺ and Ca²⁺‐activated K⁺ (K_Ca) channels. Since our previous study showed that A1‐ and A_2A‐receptor‐mediated NO release requires activation of adenylate cyclase (AC), we propose the following novel pathways. The K⁺ efflux resulting from A₁‐receptor …