NITRIC oxide (NO) and adenosine are involved in coincident CNS functio
ns, including long-term potentiation, neuronal protection, neurotoxici
ty and cerebral blood flow. We tested the hypothesis that glia may act
as a cellular link between the two, through adenosine-induced NO rele
ase from astrocytes. A direct NO measuring system was used, allowing t
he kinetics of NO release to be measured. Our results show that adenos
ine, acting through purinoceptors, causes NO release from cultured cor
tical astrocytes. Mobilization of calcium from intracellular stores ra
ther than influx is involved in the adenosine-induced activation of NO
synthase. These results demonstrate a possible interaction between ad
enosine and NO in cerebrovascular physiology and neurotoxicity.