Background: Capsaicin has been found to act on the capsaicin sensitive afferent nerves in animal experiments.
Aim: The specific action of capsaicin on sensory afferent nerves affecting gastrointestinal (GI) functions was investigated in human GI physiology and pathology using pharmacological approaches.
Materials and methods: Observations were carried out in 98 normal healthy human subjects and in 178 patients with different gastrointestinal diseases (gastritis, erosions, ulcer, polyps, cancer, inflammatory bowel diseases, colorectal polyps, cancers). The gastric secretory responses and their chemical composition, gastric emptying, sugar loading test, gastric transmucosal potential difference (GTPD) were investigated following with administration of (a) capsaicin alone, (b) ethanol alone or with capsaicin, and (c) indomethacin-induced gastric mucosal microbleeding with or without capsaicin, both before and after 2 weeks capsaicin treatment. Immunohistochemical investigations were performed to establish the presence of the capsaicin (vanillinoid) receptor (TRVP1), CGRP and SP in the whole GI tract. Conventional molecular pharmacological methods were applied to study the effects of capsaicin and other drugs for their inhibitory effects on the gastric basal acid output.
Results: Capsaicin decreased the gastric basal output, enhanced the "non parietal" (buffering) component of gastric secretory responses, gastric emptying, release of glucagon. Capsaicin prevents the indomethacin- and ethanol-induced gastric mucosal injury, while capsaicin itself enhanced the gastric transmucosal potential difference (GTPD). The capsaicin reactive receptors, TRVP1, CGRP, SP were detected in the GI mucosa in patients with different GI disorders, but their presence varied in acute and chronic GI disorders.
Conclusion: Application of capsaicin offers a new research tool for understanding the vanilloid-related events of human GI functions in relation to normal physiology and in disease states and the use of pharmacological agents affecting these receptor mediated changes.