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¹ Department of Physiology, The Medical School, Birmingham B15 2TT, UK

The role of adenosine in exercise hyperaemia has been controversial. Accumulating evidence now demonstrates that adenosine is released into the venous efflux of exercising muscle and that adenosine is responsible for 20–40% of the maintained phase of the muscle vasodilatation that accompanies submaximal and maximal contractions. This adenosine is mainly generated from AMP that is released from the skeletal muscle fibres and dephosphorylated by ecto 5'nucleotidase bound to the sarcolemma. During exercise, the concentration of ecto 5'nucleotidase may be increased by translocation from the cytosol, while release of AMP and affinity of ecto 5'nucleotidase for AMP are increased by acidosis. The adenosine so formed, acts on extraluminal A_2A receptors on the vascular smooth muscle. In addition, ATP is released from red blood cells into the plasma during exercise, in association with the unloading of O₂ from haemoglobin, while ATP and adenosine may be released from endothelium as a consequence of local hypoxia. It is unlikely that this intraluminal ATP, or adenosine, contributes significantly to exercise hyperaemia, for muscle vasodilatation induced by intraluminal ATP or adenosine is strongly nitric oxide dependent, while vasodilatation induced by adenosine in hypoxia is mediated by A₁ receptors. Neither is a recognized feature of exercise hyperaemia.

(Received 15 May 2007; accepted after revision 3 July 2007; first published online 5 July 2007)
Corresponding author J. M Marshall: Department of Physiology, The Medical School, Birmingham B15 2TT, UK. Email: j.m.marshall{at}bham.ac.uk

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