In this article, we have presented evidence that vagal capsaicin-sensitive afferent fibers are involved in the regulation of gastric mucosal and motor function. Gastric acid secretion stimulated by gastric distension, histamine and central injection of TRH analog are all partly dependent on vagal capsaicin-sensitive afferent mechanisms. It is possible that as vagal efferent activity releases histamine, the common final pathway is the reduction in the response to histamine. At present, it is unclear as to the mechanism by which capsaicin-sensitive afferents are involved in the secretory response to histamine. With regard to the gastric acid and mucosal blood flow responses to TRH, it is not clear whether the sensory neurons represent a component of the efferent pathway that is activated by TRH or whether their role is to set the sensitivity of, or exert feedback control on this efferent pathway. As perineural capsaicin application decreases peptide content in the peripheral terminal fields of sensory neurons and these peptides may produce local effector functions within the tissue, it is possible that alterations in the gastric responses to TRH result from a decrease in the local effector functions of vagal neurons. From the experiments on electrical stimulation of the vagus nerve, it is evident that antidromic stimulation of vagal afferents can stimulate gastric mucosal blood flow, although under these experimental conditions there was no evidence for a capsaicin-sensitive stimulation of gastric acid secretion. The physiological relevance of this stimulation of gastric mucosal blood flow is at present unclear, but it is possible that physiological stimuli, such as distension or nutrients, may stimulate afferents and signal for an increase in gastric mucosal blood flow. In addition, pathophysiological or noxious stimulation of vagal afferents may also signal for an increase in gastric mucosal blood flow and may play a role in the response of the mucosa to injury.