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% O2) and reduced (15, 10, 5, or 0% O2) concentrations of O2. The vessels exhibited a significant dilation in response to reduced PO2, which could be inhibited by selective perfusion of the lumen with 21% O2 PSS, endothelial removal, and 1 microM indomethacin, but was unaffected by the nitric oxide synthase inhibitor N omega-nitro-L-arginine (10 microM). Contraction of the arteries in response to 50 mM K+ was inhibited by 0% O2, whereas agonist (norepinephrine and serotonin)-induced contractions and pressure-induced myogenic responses were insensitive to reduced PO2. These results suggest that 1) skeletal muscle resistance arteries are intrinsically sensitive to reduced PO2 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 PO2 in extraparenchymal resistance arteries of skeletal muscle.