Adenosine as a mediator of postcontraction hyperemia in dog gracilis muscle

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Abstract
The role of adenosine in postcontraction hyperemia (PCH) following sustained, maximal isometric contractions was studied in free-flowing dog gracilis muscles. The hemodynamic responses to contraction were exmained in the presence and absence of dipyridamole (an adenosine transport inhibitor), erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA, an adenosine deaminase inhibitor), or .alpha.,.beta.-methyleneadenosine-5''-diphosphate (AOPCP, an inhibitor of 5''-nucleotidase). Each muscle was stimulated to contract for 1, 3, 5 and 10 s during saline and drug infusions. For each contraction, the tension-time integral (TT), excess flow (EQ) and excess O2 consumption (E.ovrhdot.VO2) were computed. Linear regression analyses were then performed on EQ vs. TT, E.ovrhdot.VO2 vs. TT and EQ vs. E.ovrhdot.VO2. An alteration of the PCH response by the drug was determined as any significant change from the saline control in the slope of the linear regression of EQ vs. E.ovrhdot.VO2. Dipyridamole and EHNA caused increases of 73 and 48%, respectively, in the slope of EQ vs. E.ovrhdot.VO2, whereas AOPCP decreased the slope by 41%. The changes in the PCH produced by these drugs are consistent with the hypothesis that an increase in interstitial adenosine during muscular contraction contributes to PCH.