Introduction Human saliva has a high nitrite concentration from the entero-salivary recirculation of dietary nitrate. Swallowed nitrite reacts with gastric acid to form nitric oxide (NO) at the gastro-oesophageal junction. This may contribute to the pathogenesis of reflux disease. NO has been shown to reduce lower oesophageal sphincter (LOS) pressure, impair oesophageal clearance and may be the final mediator in the production of transient lower oesophageal sphincter relaxations (TLOSRs).
Aims To determine (1) whether nitrite in saliva increases oesophageal acid exposure and (2) whether nitrite in swallowed saliva modifies the manometric characteristics of the LOS and distal oesophagus.
Methods 20 asymptomatic subjects (11 males) were studied. Each underwent endoscopy to document normal anatomy. On four separate days, high-resolution manometry and pH were performed during 15 min fasting and for 90 min following a standardised meal. Postprandially, solutions containing 0, 0.286, 2 and 14 mmol/l potassium nitrite were infused into the oral cavity. Solutions were randomised and double-blinded. Saliva was collected at baseline, 30, 60 and 90 min following the meal. Nitrite concentrations were quantified by Griess reaction. Acid exposure was calculated as per cent time pH<4. The number of reflux events was calculated and reflux event characteristics (duration and nadir pH) recorded. TLOSRs were determined using established criteria. Mean LOS pressure, peristaltic wave velocity and peristaltic amplitude were also calculated. To adjust for multiple comparisons the Bonferroni method was used with p<0.017 considered significant. Results are medians and ranges unless stated.
Results Salivary nitrite concentrations at 60 min were 24.35 μmol/l (3.86–65.46), 80.42 μmol/l (20.88–158.79), 358.4 μmol/l (118.2–726.6) and 2694 μmol/l (600–8087) for the solutions containing 0, 0.286, 2 and 14 mmol/l nitrite, respectively. There was no difference in acid exposure between the control and the nitrite-containing solutions (p>0.04). There was no difference in the number (p>0.05), duration (p>0.4) or nadir pH (p>0.2) of reflux events. The mean number of TLOSRs and the reduction in postprandial LOS pressure were similar (p>0.04 and p>0.07). There was no difference in peristaltic wave velocity or amplitude (p>0.1 and p>0.6).
Conclusion Despite an excellent range of salivary nitrite concentrations, over and beyond the normal physiological range, no difference in oesophageal acid exposure or oesophageal motility was seen between the control solution and those containing nitrite. These findings suggest that salivary nitrite does not potentiate oesophageal reflux.
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