Figure 4:  Mechanism of ADO release and regulation by ADO kinase (AK).

Following cellular injury, extracellular concentrations of  ADO are markedly increased via an enhanced release of intracellular ADO and/or ATP which is rapidly degraded to ADO by ectonucleotidases.  Once in the extracellular space, ADO activated cell surface P1 receptors leading to a variety of homeostatic neuromodulatory processes.  Both in vitro and in vivo data (see text) indicate that AK exerts a primary role in the regulation of intracellular ADO levels.

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published 2000