Nitric oxide does not mediate arteriolar oxygen reactivity.

Endothelium-derived relaxing factor, which is believed to be nitric oxide (NO), mediates vasodilation of arteries perfused with hypoxic solutions. The purpose of the present study was to determine if NO mediates the response of arterioles in the hamster cheek pouch to changes in superfusion solution PO2. This was accomplished by comparison of constriction of fourth order arterioles to increases in superfusate PO2 before and during superfusion with NG-nitro-L-arginine (L-NAG), a stereospecific inhibitor of NO synthesis. The efficacy of L-NAG was assessed by comparison of dilations induced by topical application of methacholine (MCH), an endothelium-dependent vasodilator. We found that 10-15 min superfusion with 30 microM L-NAG significantly inhibited MCH-induced arteriolar dilation. However, this concentration of L-NAG had no significant effect on resting arteriolar diameters, O2-induced constrictions, constrictions induced by phenylephrine or dilations induced by sodium nitroprusside (SNP). Increasing the concentration of L-NAG to 100 microM similarly inhibited MCH-induced dilations, but did not affect SNP reactivity and may have increased vasoconstriction induced by O2. Thus, effective inhibition of NO synthesis in the hamster cheek pouch does not inhibit responses to elevated oxygen. Therefore NO does not mediate arteriolar O2 reactivity in this tissue. Furthermore, there is little evidence for tonic modulation of arteriolar reactivity by NO in the microvessels observed in this study.