AIM: We examined the effect of H₂S on duodenal HCO₃⁻ secretion in rats and investigated the mechanism involved in this response. METHODS: Animals were fasted for 18 h and anaesthetized with urethane. A duodenal loop was perfused with saline, and HCO₃⁻ secretion was measured at pH 7.0 using a pH stat-method. The loop was perfused at a rate of 0.2 mL min⁻¹ with NaHS (H₂S donor: 0.1-1 mm) for 5 min or 10 mm HCl for 10 min. Indomethacin or l-NAME [nitric oxide (NO) synthase inhibitor) was given s.c. 30 min or 3 h, respectively, before NaHS or acidification, while glibenclamide (K(ATP) channel blocker) or propargylglycine (cystathionine-g-lyase inhibitor) was given i.p. 30 min before. RESULTS: Mucosal perfusion with NaHS dose dependently increased the HCO₃⁻ secretion, and this effect was significantly attenuated by indomethacin and l-NAME as well as by sensory deafferentation, but not by glibenclamide. Mucosal prostaglandin E₂ (PGE₂) production and luminal release of NO were both increased by NaHS perfusion. Mucosal acidification stimulated HCO₃⁻ secretion concomitant with an increase in PGE₂ and NO production, and these responses were mitigated by propargylglycine. The duodenal damage induced by acid (100 mm HCl for 4 h) was aggravated by pre-treatment with propargylglycine. CONCLUSION: These results suggest that H₂S increases HCO₃⁻ secretion in the rat duodenum, and that this action is partly mediated by PG and NO as well as by capsaicin-sensitive afferent neurones. It is assumed that endogenous H₂S is involved in the regulatory mechanism of acid-induced HCO₃⁻ secretion and mucosal protection in the duodenum.
AIM: We examined the effect of H₂S on duodenal HCO₃⁻ secretion in rats and investigated the mechanism involved in this response. METHODS: Animals were fasted for 18 h and anaesthetized with urethane. A duodenal loop was perfused with saline, and HCO₃⁻ secretion was measured at pH 7.0 using a pH stat-method. The loop was perfused at a rate of 0.2 mL min⁻¹ with NaHS (H₂S donor: 0.1-1 mm) for 5 min or 10 mm HCl for 10 min. Indomethacin or l-NAME [nitric oxide (NO) synthase inhibitor) was given s.c. 30 min or 3 h, respectively, before NaHS or acidification, while glibenclamide (K(ATP) channel blocker) or propargylglycine (cystathionine-g-lyase inhibitor) was given i.p. 30 min before. RESULTS: Mucosal perfusion with NaHS dose dependently increased the HCO₃⁻ secretion, and this effect was significantly attenuated by indomethacin and l-NAME as well as by sensory deafferentation, but not by glibenclamide. Mucosal prostaglandin E₂ (PGE₂) production and luminal release of NO were both increased by NaHS perfusion. Mucosal acidification stimulated HCO₃⁻ secretion concomitant with an increase in PGE₂ and NO production, and these responses were mitigated by propargylglycine. The duodenal damage induced by acid (100 mm HCl for 4 h) was aggravated by pre-treatment with propargylglycine. CONCLUSION: These results suggest that H₂S increases HCO₃⁻ secretion in the rat duodenum, and that this action is partly mediated by PG and NO as well as by capsaicin-sensitive afferent neurones. It is assumed that endogenous H₂S is involved in the regulatory mechanism of acid-induced HCO₃⁻ secretion and mucosal protection in the duodenum.