Adenosine-induced release of nitric oxide from cortical astrocytes

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