Capsaicin-induced hyperemia in the stomach: possible contribution of mast cells.

Topical application of capsaicin to the gastric mucosa results in marked hyperemia as a consequence of the release of vasoactive neuropeptides from sensory afferent neurons. Because many of these neuropeptides have the capacity to induce mast cell degranulation, we investigated the possible contribution of mast cells to capsaicin-induced hyperemia. Application of capsaicin to the gastric mucosa of normal rats resulted in a concentration-dependent increase in blood flow. In rats in which mastocytosis was induced by prior infection with Nippostrongylus brasiliensis, the hyperemic responses to capsaicin were significantly greater than in control rats. This augmented hyperemic response could be significantly attenuated by pretreatment with a histamine H1-receptor antagonist (pyrilamine) or with a mast cell stabilizer (doxantrazole). Depletion of mucosal mast cells through treatment with dexamethasone also significantly reduced the hyperemic response to capsaicin. Hyperemic response to capsaicin in normal rats and in rats with mucosal mastocytosis could be completely abolished by pretreatment with ruthenium red or prior ablation of the sensory afferent neurons with capsaicin. These results suggest that in rats with gastric mastocytosis, sensory neuron-dependent activation of mast cells contributes to the hyperemic response to topical capsaicin. These findings are therefore consistent with the hypothesis that there is communication between nerves and mast cells in the gastric mucosa, at least in rats previously infected with N. brasiliensis.