Abstract
To the Editor: Webb and Milsom et al1 present the intriguing finding that endothelial nitric oxide synthase (eNOS) in human umbilical vein endothelial cells (HUVECs) and potentially RBCs is responsible under hypoxic conditions for nitrite (NO2•) reduction to nitric oxide (NO). Based on several practical and theoretical points of view, the conclusions that the authors draw regarding their data are flawed. It is important that these are considered by the wider Circulation Research readership. The authors conclude that lack of oxygen (O2) availability to eNOS promotes NO2• reduction to NO. Whereas the RBC experiments involve measurement of NO produced by RBC under nitrogen and acidic conditions, the HUVEC experiments were carried out at 5% O2 and 5% CO2 (refer to online data supplement that accompanies the article for details). Although there is no question 5% …
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