The effects of adenosine analogues on the electrically-evoked norepinephrine(NE) release and the influence of ischemia on the effects were studied in the rat hippocampus. Slices from the rat hippocampus were equilibrated with 0.1μM [³H]-norepinephrine and the release of the labelled product, [³H]-NE, was evoked by electrical stimulation(3 Hz, 2 ms, 5 VCm₃₄₀and rectangular pulses for 90 sec), and the influence of various agents on the evoked tritium-outflow was investigated. Ischemia(15min with 95% N₂ +5% CO₂) increased both the basal and evoked NE release. These increases were abolished by addition of glucose into the superfused medium, and they were significantly inhibited either by 0.3μM tetrodotoxin pretreatment or by removing Ca⁺⁺ in the medium. MK-801(1~10μM), a specific NMDA receptor antagonist, and glibenclamide (1μM), a K⁺-channel inhibitor, neither alter the evoked NE release nor affected the Ischemia-Induced increases in NE release. However, polymyxin B(0.03 mg), a specific protein kinase C inhibitor, inhibited the effect of ischemia on the evoked NE release. Adenosine and N⁶-cyclopentyladenosine decreased the NE release in a dose-dependent manner in ischemic condition, though the magnitude of inhibition was far less than those in normal (normoxic) condition. Also the treatment with 5μM DPCPX, a potent A₁-adenosine receptor antagonist did not affect the ischemia-effect. These results suggest that the evoked-NE release is potentiated by ischemia, and this process being most probably mediated by protein kinase C, and that the decrease of NE release mediated through A₁-adenosine receptor is significantly inhibited in ischemic state.