The dependence of adenosine release on blood flow was investigated in greyhounds anaesthesized with sodium pentobarbitone and artificially ventilated. The gracilis muscles were neurally and vascularly isolated, and perfused at constant flow rates of 42% (low), 89% (medium) or 132% (high) of their maximum free flow during contraction induced by stimulation of the motor nerve. Stimulation produced contractions whose force declined from 716 +/- 60 to 464 +/- 46 g (100 g)-1 over 10 min. Resting perfusion pressure increased in line with the flow rate, but the fall in resistance accompanying contractions varied reciprocally with the flow (57 +/- 2.9, 39.6 +/- 6.6 and 15.3 +/- 5.6% at low, medium and high flows respectively). Venous PO2 decreased during contraction to 26.6 +/- 6.2 mmHg at 'low', 31.5 +/- 5.1 mmHg at 'medium' and 37.2 +/- 1.7 mmHg at 'high' flows. Venous plasma adenosine concentration increased significantly above resting levels during contraction at all flow rates. Adenosine release at low flow (12.0 +/- 2.7 nmol min-1 (100 g)-1) was significantly greater than that at medium or high flows (5.6 +/- 1.3 and 4.1 +/- 1.3 nmol min-1 (100 g)-1 respectively), but the latter were not different from each other. There was no correlation between adenosine release and either venous oxygen tension during muscle contraction or the ratio of oxygen supply to free-flow oxygen consumption. These data suggest that the mechanism underlying adenosine release during muscle contraction may be independent of oxygen lack.