抄録
Nitric oxide (NO) is known to be involved in nicotine-induced increases in cerebral cortical blood flow. To study the exact mechanism(s) of nicotine-induced increases in cerebral blood flow, we measured blood flow in the left hippocampus of the rat using a laser Doppler probe and NO current in the right hippocampus using an NO-selective electrode. Nicotine increased blood flow and decreased NO production in the hippocampus. This indicates that this potentiation is not due to NO-mediated increases in blood flow. Because nicotine has been reported to release adenosine in rat cerebral cortex, we examined the effects of adenosine-related compounds on the responses induced by nicotine in blood flow and NO production. The nonselective adenosine receptor antagonist theophylline attenuated not only the nicotine-induced increases in blood flow but also the nicotine-induced decreases in NO production. The adenosine uptake inhibitor propentofylline, on the other hand, facilitated the nicotine-induced increases in blood flow, but it reduced the nicotine-induced decreases in NO formation. These results suggested that adenosine mediates nicotine-induced increases in hippocampal blood flow. [Jpn J Physiol 54 Suppl:S101 (2004)]
