RESPONSE OF EXTRAPARENCHYMAL RESISTANCE ARTERIES OF RAT SKELETAL-MUSCLE TO REDUCED PO2

Isolated resistance arteries from the gracilis muscle of rats were simultaneously perfused and superfused with physiological salt solution (PSS) equilibrated with control (21% O-2) and reduced (15, 10, 5, or 0% O-2) concentrations of O-2. The vessels exhibited a significant dilation in response to reduced Po-2, which could be inhibited by selective perfusion of the lumen with 21% O-2 PSS, endothelial removal, and 1 mu M indomethacin, but was unaffected by the nitric oxide synthase inhibitor N-omega-nitro-Larginine (10 mu M) Contraction of the arteries in response to 50 mM K+ was inhibited by 0% O-2, whereas agonist (norepinephrine and serotonin)-induced contractions and pressure-induced myogenic responses were insensitive to reduced Po-2. These results suggest that 1) skeletal muscle resistance arteries are intrinsically sensitive to reduced Po-2 independent of parenchymal cell influences, 2) inhibition of resting tone in these vessels is mediated by an endothelium-derived product of the cyclooxygenase pathway, and 3) various forms of contractile activation are not equally sensitive to inhibition by reduced Po-2 in extraparenchymal resistance arteries of skeletal muscle.