Role of capsaicin-sensitive sensory nerves in acid-induced bicarbonate secretion in rat stomach

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Abstract
The effect of capsaicin-sensitive afferent nerves on the alkaline secretory response induced by mucosal acidification was investigated in theex vivo stomachs of anesthetized rats. The stomach was mounted on a Lucite chamber and perfused with saline (pH 4.5) in the absence of acid secretion (omeprazole pretreatment: 60 mg/kg, intraperitoneal), and luminal pH and transmucosal potential difference (PD) were monitored simultaneously. Under these conditions the gastric mucosa responded to intravenous infection of prostaglandin E2 (PGE2: 300 μg/kg) and mucosal acidification (0.2 N HCl for 10 min) by a significant increase of pH with a slight decrease of PD; the HCO3− output was 9.2±0.7 μmol and 8.4±0.8 μmol, respectively. The increased pH and HCO3− responses were significantly inhibited by prior administration of indomethacin (5 mg/kg, subcutaneously) or chemical deafferentation following capsaicin injections (total dose: 100 mg/kg, subcutaneously), whereas those induced by PGE2 remained unchanged after either treatment. On the other hand, the mucosal application of capsaicin (0.3–6 mg/ml) increased the luminal pH and HCO3− output in a concentration-related manner, and this action was also significantly attenuated by either indomethacin or chemical deafferentation of capsaicin-sensitive sensory neurons. These results suggest that capsaicin-sensitive sensory nerves may be involved in the mechanism of acid-induced HCO3− secretion in the stomach, in addition to endogenous PGs, and these two pathways may interact somewhere in the stimulatory process.