Effect of oxygen tension on regulation of arteriolar diameter in skeletal muscle in situ

Skeletal muscle arterioles are known to constrict upon elevation of ambient PO₂. While several studies have shown that the endothelium plays an important role in this response. it is not clear how this response is mediated. We examined the oxygen-induced constriction of arterioles in the rat spinotrapezius muscle. Elevation of superfusion solution PO₂ from about 15 to 150 mm Hg caused arteriolar constriction by 25% (±3%, n = 18). Inhibition of prostaglandin synthesis by superfusion of indomethacin (30 μM) produced vasoconstriction by 28% (±9.5%, n = 5), but left the PO₂ response unaffected. Blockade of the synthesis of endothelium-derived relaxing factor (EDRF) by N^G-nitro-L-arginine (L-NNA, 35 mg/kg iv) caused arteriolar constriction by 31% (±8%, n = 8). During application of L-NNA, the constrictor response to PO₂ elevation was reduced to 3 ± 2%. Administration of superoxide dismutase (SOD, 80,000 U/kg iv) did not affect the PO₂ response. It is concluded that in small arterioles of skeletal muscle both EDRF and prostanoids sustain a significant basal dilatation. The dilatory effects of EDRF but not of prostaglandins are strongly dependent on PO₂. The vasoconstriction in response to high ambient PO₂ is not due to EDRF breakdown during its diffusion from endothelial to smooth muscle cells.