Sure thing- here are a coupls good abstracts explaining how it works:
Tannenbaum et al. 1984
Pharmacokinetics of nitrate in humans: role of gastrointestinal absorption and metabolism
Abstract
A model to describe the response of the blood pool to an oral dose of nitrate in humans has been developed. The permeability-area product of the small intestine to nitrate was estimated by comparing simulations from a three-compartment model with published data for blood nitrate concentration following nitrate ingestion. The transport of nitrate firom the bloodstream to the lumen of the large intestine and the metabolism of nitrate by enteric bacteria were examined by including an additional compartment representing the large bowel. The simulations indicate that the bacteria of the large intestine may be responsible for about half of the extrarenal removal of nitrate from the body. This prediction was tested experimentally by comparing the urinary recoveries of 15NO3− in conventional and germfree rats following an i.p. dose of Na15Na3. The mean urinary recovery in gennfree rats (71% of dose) substantially exceeded that in rats with conventional bacterial flora (54%). This suggests that of the 40 – 45% of a nitrate dose that is metabolized in the body rather than excreted in urine as nitrate, approximately naif is metabolized by mammalian processes and approximately half by enteric bacteria. This conclusion is consistent with that obtained from our pharmacokinetic model of nitrate in humans.
Am J Clin Nutr. 1991 Jan;53(1 Suppl):247S-250S.
Inhibition of nitrosamine formation by ascorbic acid.
Tannenbaum SR, Wishnok JS, Leaf CD.
Source Massachusetts Institute of Technology, Cambridge 02139.
Abstract
Nitrosation occurs under a wide variety of conditions by reaction of most types of amines with any of a large number of nitrosating species. Nitrite can be formed in vivo via bacterial reduction of nitrate and by activated macrophages and endothelial cells. The mechanism of nitrite formation by mammalian cells is via enzymatic oxidation of arginine to NO followed by oxidation to N2O3 and N2O4. Nitrosatable amines are found in many foods and some, eg, dimethylamine, are synthesized in the body. Precursors of N-nitroso compounds are thus almost constantly present together under favorable reaction conditions in vivo and there is, consequently, considerable interest concerning possible human health risks arising from endogenous formation of this class of compounds. Among many nitrosation inhibitors, most attention has focused on ascorbic acid, which reacts with many nitrosating agents and which is virtually nontoxic. This presentation discusses the chemistry of ascorbic acid inhibition of nitrosation reactions.
With this in mind, we can use creatine nitrate as an example. When the salt is ingested, it immediately dissociates into a molecule of creatine, and a molecule of nitrate. Creatine is readily assimilated, and nitrate has two routes once ingested- it can be converted in the stomach to nitric oxide- hence the claim of the "Reverse N.O. Pathway", or it can be converted to nitrite. NOS is required in the conversion of arginine to NO, but is not required in this situation. Nitrite is a relatively potent and fast vasodilator at near-physiological concentrations, and nitrite functions as an endocrine reservoir of nitric oxide,so it is is also helpful in maintaining nitric oxide levels. Nitrites are normally reduced to nitric oxide via intravascular reactions with hemoglobin (a component found in red blood cells) and with certain reductive compounds (this is why supplemental iron is needed when taking nitrates). However, in absence of these reductive compounds, nitrites can be converted into nitrosating agents. This can cause some issues- but nitrosation can be prevented by taking in vitamin C along with the nitrates (see above).
