Adenosine and active hyperemia in dog skeletal muscle.

Adenosine as a possible mediator of active hyperemia in skeletal muscle was studied in hindlimbs of dogs. Sciatic nerve stimulation decreased vascular resistance to 55 +/- 5% (mean +/- SE) of the control value in hindlimbs perfused at a constant flow rate (61 +/- 6 ml/min). Venous plasma K+ concentrations were elevated after 2 min (from 4.0 +/- 0.2 to 4.8 +/- 0.2 meq/liter; P is less than 0.005) and 20 min (4.7 +/- 0.2 meq/liter; P is less than 0.001) of contraction, but the arteriovenous difference in plasma osmolality was changed only after 2 min of contraction (from -3.0 +/- 0.6 to -7.2 +/- 0.8 mosmol/kg H2O; P is less than 0.001). The muscle adenosine contents were not significantly elevated after 5 min of contraction, but were increased after 10 min (from 1.97 +/- 0.33 to 8.35 +/- 0.97 nmol/g; P is less than 0.05) and 25 min (from 1.64 +/- 0.22 to 7.57 +/- 2.20 nmol/g; P is less than 0.05) of contraction. Thirty minutes after contraction had ceased, the adenosine contents were significantly below control values (from 2.22 +/- 0.59 to 1.51 +/- 0.40 nmol/g; P is less than 0.005). Venous plasma adenosine concentrations did not increase during muscle contraction. No relationship was found between the increase in the plasma inorganic phosphate level and the activity of the muscles. These data indicate that the adenosine content of skeletal muscle is increased by contraction, and support the concept that adenosine may be a mediator of sustained active hyperemia.