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Capsaicin decreased the gastric basal output, enhanced the "non-parietal" (buffering) component of gastric secretory responses, and gastric emptying, and the release of glucagon. Capsaicin prevented the indomethacin- and ethanol-induced gastric mucosal damage; meanwhile capsaicin itself enhanced (GTPD). Capsaicin prevented the indomethacin-induced gastric mucosal microbleeding. The expression of TRVP1 and CGRP increased in the gastric mucosa of patients with chronic gastritis (independently of the presence of Helicobacter pylori infection), and the successfully carried out eradication treatment. The human first phase examinations (the application of acetylsalicylic acid (ASA), diclqfenac, and naproxen together with capcaicinoids) (given in doses that stimulate capsaicin-sensitive afferent vagal nerves) showed no change in the pharmacokinetic parameters of ASA and diclofenac and the ASA and diclofenac-induced platelet aggregation.