ISCHEMIC SKELETAL-MUSCLE HYPEREMIA IN THE ANESTHETIZED CAT - NO CONTRIBUTION OF A(2A) ADENOSINE RECEPTORS

1. The present study investigated the contribution of the A(2A) adenos ine receptor subtype to the functional hyperaemia response evoked by m uscle contraction in anaesthetized cats when muscle blood flow was lim ited. 2. Application of a stenosis reduced the hindlimb blood flow at rest from 9.67 +/- 1.80 to 5.53 +/- 0.91 ml min(-1) (kg body mass)(-1) and during muscle contraction from 36.80 +/- 2.55 to 11.11 +/- 1.19 m l min(-1) (kg body mass)(-1) (P < 0.001). The force produced by the ex tensor digitorum longus and tibialis anterior (EDL-TA) muscle groups w as also reduced, from 9.66 +/- 0.56 to 4.10 +/- 0.4 N (kg muscle mass) (-1) (P < 0.01). 3. The selective A(2A) adenosine receptor antagonist ZM241385 (3 mg kg(-1), I.V.) had no effect upon the hindlimb vascular conductance or muscle contraction responses in the presence of the flo w-limiting stenosis. 4. In contrast, in the absence of the flow restri ction the vascular conductance response was reduced by 27.5 +/- 5.0% ( P < 0.05), whilst the isometric force produced by the EDL-TA muscle gr oup was unaffected (pre- vs. post-contraction, 5.8 +/- 0.8 vs. 4.8 +/- 1.0 N (kg muscle mass)(-1) contraction). Oxygen consumption by the co ntracting hindlimb muscles was maintained (1.71 +/- 0.25 vs. 1.69 +/- 0.26 ml min(-1) (kg body mass)(-1)) by an increase in the oxygen extra ction (51.9 +/- 4.9 vs. 66.2 +/- 6.1%; P < 0.01). 5. These results con firm previous data showing that adenosine, acting at the A(2A) recepto r subtype, can contribute up to 30% of the functional hyperaemia respo nse in the hindlimb of anaesthetized cats under free flow conditions. However, when blood flow is limited by a stenosis, antagonism of the A (2A) adenosine receptor does not affect functional hyperaemia.