Synthetic nitric oxide donors are known to protect the gastric mucosa from damage and dietary nitrate is known to release NO in the stomach. Mast cells have been found to be involved in gastric mucosal damage in humans or in rodents, and recent studies have pointed out the possibility of nitric oxide from endogenous or exogenous origin to modulate mast cell reactivity. This study aimed to determine whether the protective effect afforded by dietary nitrate against gastric mucosal damage was linked to mast cell stabilization. Mast cell involvement in iodoacetamide-induced gastritis was investigated in rats receiving oral administration of iodoacetamide together with the mast cell stabilizer doxantrazole (ip) or its solvent. The effects of dietary nitrate on mast cells during gastritis were investigated in rats receiving iodoacetamide orally, associated or not with KNO₃. Control groups were given water instead of iodoacetamide either with or without KNO₃, doxantrazole or its solvent. After sacrifice, blood samples were taken to determine RMCP II serum level and the stomach was resected in order to determine myeloperoxidase (MPO) activity and mucosal mast cell (MMC) number. Iodoacetamide significantly increased gastric MPO activity but did not modify RMCP II serum level or MMC number. Doxantrazole and KNO₃ significantly reduced iodoacetamide-induced increase in gastric MPO activity, increased MMC number, and decreased RMCP II serum level in basal conditions. Only doxantrazole was able to modify all parameters under inflammatory conditions. These results suggest that nitric oxide released by dietary nitrate in the stomach stabilizes mast cells in basal conditions but exerts its protective effect against experimental gastritis through other pathways.