ROLE OF ENDOTHELIAL FACTORS IN ACTIVE HYPEREMIC RESPONSES IN CONTRACTING CANINE MUSCLE

We investigated whether endothelium-derived relaxing factor (EDRF) and prostaglandins, which may be released under conditions of increased b lood flow, contribute to the active hyperemia in contracting muscle of anesthetized dogs. The venous outflow from the left gastrocnemius mus cle was isolated and measured. The tendon was cut and placed in a forc e transducer. One group served as a control (Con; n = 9); EDRF synthes is was inhibited using N-w-nitro-L-arginine methyl ester (L-NAME) in a second group (n = 9), and a third group (n = 7) received L-NAME and i ndomethacin (L-NAME + Indo) to inhibit prostaglandin synthesis. After resting measurements, the distal end of the cut sciatic nerve was stim ulated to produce isometric contractions at 1, 2, 4, and 6 twitches/s for 6-8 min, separated by 25-min recovery periods. Blood flow and O-2 uptake increased linearly from resting values of 11.8 +/- 2.4 and 0.3 +/- 0.05 ml . 100 g(-1). min(-1), respectively, to maximal values of 8 4.2 +/- 5.1 and 11.1 +/- 0.7 ml . 100 g(-1). min(-1) in the Con group; neither these values nor those for tension development were different from values observed at comparable contraction frequencies in the L-N AME and L-NAME + Indo groups. At rest, resistance was greater (P < 0.0 5) in both the L-NAME and L-NAME + Indo groups compared with Con, the highest value (P < 0.05) occurring in the L-NAME + Indo group. Muscle resistance decreased (P < 0.05) in all groups at all contraction frequ encies; the values were not different among the three groups. Because differences in resting vascular resistance were abolished even at 1 tw itch/s, we believe that endothelial factors, which modulate vascular t one at rest, do not contribute to active hyperemia.