Abstract
In rat brain astroglia-enriched cultures long-term treatment with interleukin-1β induces NO release and stimulation of soluble guanylyl cyclase. The cGMP formed is recovered in the extracellular medium but not in the cell monolayer. The interleukin-1β effect is mediated by type I receptor and potentiated by interferon-γ. In cells treated with bacterial endotoxin a larger NO-dependent cGMP accumulation occurs only intracellularly, however a significant cGMP egression is observed when cells are co-treated with interleukin-1β. The non-selective anion transport inhibitors probenecid and verapamil block cGMP efflux, indicating that interleukin-1β stimulates a cGMP transporter.
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