Confusion About Nitrite vs. Nitrite+Nitrate (NOx) in the Evaluation of eNOS-Derived NO

This is an interesting article, and the authors claim that an acute increase in the plasma nitrite [(NO2)-], providing that its levels are measured locally in the venous blood in response to ACh infusion in the presence of L-NMMA, reflects an increase in NO release due to eNOS activity. The authors found that the levels of nitrate [(NO3)-] or nitrite+nitrate [(NO2)- and (NO3)-], sometimes expressed as "NOx," did not increase in response to the ACh+L-NMMA infusion, and so one message is that nitrate levels don't correlate well with eNOS activity. And I understand what they're using as a rationale for excluding iNOS-derived NO as a factor that might have contributed to the nitrite levels following ACh. They're saying that an increase in plasma nitrite, in the absence of some information about the conditions under which the increase occurred (in contrast to the controlled conditions in this experiment), can, in fact, be the result of both iNOS and eNOS activities. They rule out a contribution from iNOS by looking at the low concentration of nitrite, and I understand that (they say that the increase in nitrite would have been larger, had it occurred via iNOS activity).

But I don't understand what they mean when they say that infusing ACh+L-NMMA "unmasks the eNOS-independent" part of the ACh-induced vasodilation. I know ACh can cause vasodilation partly by releasing endothelium-derived hyperpolarizing factor, etc., but they're measuring NO increases in response to ACh+L-NMMA? I'm not even clear on what concentration they're using of L-NMMA. This article says that, depending on the concentration or preincubation time, L-NMMA can either inhibit eNOS or iNOS (http://www.ncbi.nlm.nih.gov/pubmed/7540822). It sounds like the mechanism-based inhibition of iNOS requires some time to occur, but the abstract says that iNOS can be reversibly inhibited by L-NMMA. It looks like the selectivity is concentration-dependent and also incubation-time-dependent, and I'm assuming these authors, of the article I link to below, were using a protocol for selectively inhibiting eNOS. But then where would the ACh-induced increase in nitric oxide production come from? It's an interesting article, and they talk about the way there are no red blood cells right up against the endothelial cells. The gradients in nitrite, too, are interesting, the way there's a net movement of nitrite or nitrate into and out of red blood cells. Hemoglobin and deoxyhemoglobin are major, if not the major, NO reservoirs in the blood, etc.:

http://www.pnas.org/content/98/22/12814.full (pubmed: http://www.ncbi.nlm.nih.gov/pubmed/11606734?dopt=Abstract)

My main area of reading, in this area, has been on the factors affecting iNOS activity vs. eNOS activity vs. peroxynitrite production, etc. It's more "pharmacological" different from the nitty-gritty of separating out the details of different protocols. But I know that looking at the plasma NOx level doesn't tell one much, and this article is one of many showing that. You need to look at some functional aspect of it and look at an acute change to rule out iNOS activity, etc. It's so localized, though. They talk about that in the article. It's interesting.