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In humans and other mammals, about one-quarter of all circulating inorganic nitrate (NO3−), derived from diet or oxidation of endogenous nitric oxide (NO), is actively taken up by the salivary glands and excreted in saliva (1, 2). As a result, salivary nitrate levels are 10–20 times higher than those levels found in plasma (3). The mechanism behind this massive nitrate accumulation in saliva has remained elusive. In PNAS, the work by Qin et al. (4) reports that the protein sialin can function as an effective nitrate transporter. These results are of considerable interest, especially in light of recent research suggesting a role for salivary nitrate transport and metabolism in physiological regulation of systemic NO homeostasis (5, 6). Historically, the fact that nitrate and nitrite are present in human saliva has received little attention, because no one could attribute any kind of function to these anions. However, this lack of interest ceased in the 1970s, when researchers formulated a pathophysiological model for gastric cancer based on the accumulation of nitrate in saliva (7). Commensal bacteria in the mouth reduce parts of the salivary-derived nitrate to nitrite (NO2−), and when swallowed into the acidic stomach, this nitrite yields reactive intermediates that can react with dietary compounds to promote formation of N-nitrosamines (a versatile class of carcinogens in rodents) (8). With the emergence of this theory, nitrate immediately fell into deep disgrace, and ever since that time, authorities worldwide have put strict regulations on allowable levels of nitrate in our food and drinking water (9). In the 1990s, research on nitrate took an unexpected turn when two research groups independently showed that salivary nitrate was a substrate for …

Nitrate transport in salivary glands with implications for NO homeostasis