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Experiments were performed on isolated frog sartorius muscle and in situ dog skeletal muscle to determine whether adenine nucleotides and their degradation products are released during contraction in concentrations capable of producing arteriolar dilation ATP was not detectable (>10−8M) in the bathing solution of the resting or contracting frog sartorius muscle. Inorganic phosphate (P1) in the muscle bath increased from 9 × 10−5M to 28 × 10−5M with 30 minutes of contraction (2 Hz) or with rest. With the dog hindlirnb preparation, ATP, ADP, and AMP were not detectable (>5 × 10−8M in the venous blood collected after 5 minutes of ischemic contraction whereas P1 was present at a concentration of 3.7 × 10×8M. Arterial blood levels required to elicit detectable vasodilation for ATP, ADP, AMP, and P1 were 28.7 × 10−8M, 27.1 × 10−8M 31.4 × 10−8M and 7.2 × 10−4M respectively. The adenosine concentration in dog muscle increased from 0.7 to 1.5 nmole/g with ischemic contraction, and hypoxanthine and inosine increased from 4.5 to 8.5 nmole/g and 2.0 to 5.5 nmole/g, respectively. The adenosine concentration in venous plasma collected from the hiodlimb immediately after termination of the irchemic contraction period was 2.2 × 10−7MM as compared to 0.4 × 10−7M in control venous and arterial blood samples. Hypoxanthine and inosine concentrations in venous blood increased 22- and 270-fold, respectively, foflowing ischemic contraction. The calculated interstitial fluid adenosine concentration was twice the arterial concentration of adenosine required to elicit maximal arteriolar dilation. These findings suggest that adenosine may play a role in the metabolic regulation of skeletal muscle blood flow, whereas ATP, ADP, AMP, and P1 may not.

Role of Adenine Nucleotides, Adenosine, and Inorganic Phosphate in the Regulation of Skeletal Muscle Blood Flow