Key role of mucosal primary afferents in mediating the inhibitory influence of capsaicin on vagally mediated contractions in the mouse esophagus.
There is both morphological and functional evidence that capsaicin-sensitive sensory neurons innervate the digestive tract. The possible function of these neurons in gastric ulceration and gastrointestinal motility was investigated in rats which had been systemically pretreated with capsaicin (50-125 mg/kg). It was found that capsaicin-sensitive afferent neurons do not participate in the physiologic control of gastrointestinal propulsion. However, the inhibition of gastrointestinal transit due to surgical trauma or peritoneal irritation with iodine was reduced in capsaicin-treated rats. It was concluded that capsaicin-sensitive sensory neurons may be involved in sympathetic reflex inhibition of gastrointestinal propulsion. Gastric ulceration induced by the intraperitoneal injection of indomethacin or intragastric administration of ethanol was greatly aggravated in capsaicin-treated rats. Since an involvement of the autonomic nervous system as well as of histamine and prostaglandins in this effect of capsaicin treatment could be ruled out, further support was lent to the previously proposed hypothesis that sensory nerve endings can protect the gastric mucosa against ulceration by the local release of vasodilator substances.