Reduction of the nociceptive response to gastric distension by nitrate ingestion in rats

Background: Dietary nitrates are known to produce nitric oxide in the stoma ch, which may influence gastric function. Aim: To investigate whether nitrate ingestion modifies gastric sensitivity to distension through a mechanism involving nitric oxide production, Methods: Nociception, associated with gastric distension ranging from 10 to 40 mmHg, was assessed in anaesthetized rats by the amplitude of cardiovasc ular depressor responses. Gastric volume corresponding to each distension w as recorded. The following intragastric administrations (1 mL) were perform ed before distension: water (control), KNO3, NaNO3, KCl, NaCl (all at 0.1 m mol/kg), standard food (0.5 g), sodium nitroprusside a nitric oxide donor ( 5 mg/kg), and haemoglobin, a nitric oxide scavenger (150 mg/kg) given eithe r with water or KNO3. Results: In controls, the fall in blood pressure increased from 7.8 +/- 2.0 to 31.6 +/- 2.7 mmHg at distending pressures from 10 to 40 mmHg, respectiv ely. KNO3 significantly reduced the amplitude of blood pressure response fo r the highest distending pressures (35 and 40 mmHg), while KCl induced a re duction in blood pressure response at all gastric pressures, NaNO3 and NaCl did not induce significant changes in distension-induced depressor respons es. Administration of 0.5 g of standard food or sodium nitroprusside reprod uced the effect of KNO3, which was reversed by haemoglobin. None of the com pounds modified the gastric pressure-volume relationship, except KNO3 which increased gastric volume for the lowest distending pressures, and haemoglo bin, which reduced the volume for the highest pressure. Conclusions: Ingestion of potassium nitrate reduces the sensitivity to gast ric distension, through a mechanism involving nitric oxide.