Abstract
AbstractThe article focuses on the events involving purine nucleotides and nucleosides during the initial responses of the cerebral vascular bed to ischaemia. In particular, the role of ATP released from endothelial cells which acts on P2Y‐purinoceptors, leading to production of nitric oxide and subsequent vasodilatation, will be considered. A relation between these events and the involvement of purines in the longer term degenerative consequences of ischaemia seems unlikely. © 1993 Wiley‐Liss, Inc.
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