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- W2027377685 abstract "We examined the effect of H2S on duodenal HCO 3 - secretion in rats and investigated the mechanism involved in this response. Animals were fasted overnight and anesthetized with urethane. A duodenal loop was perfused with saline, and HCO 3 - secretion was measured at pH 7.0 using a pH stat-method. The loop was perfused at a rate of 0.2 mL/min with NaHS (H2S donor) for 5 min or 10 mM HCl for 10 min. Indomethacin or l -NAME was given s.c. 30 min or 3 h, respectively, before NaHS or acidification, while glibenclamide (KATP channel blocker) or propargylglycine (cystathionine-g-lyase inhibitor) was given i.p. 30 min before. Mucosal perfusion with NaHS dose-dependently increased the HCO 3 - secretion, and this effect was significantly attenuated by indomethacin and l -NAME as well as sensory deafferentation, but not by glibenclamide. Mucosal PGE2 and NO production were both increased by NaHS perfusion. Mucosal acidification stimulated HCO 3 - secretion concomitant with 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 pretreatment with propargylglycine. These results suggest that H2S increases HCO 3 - secretion in the duodenum, and this action is partly mediated by PG and NO as well as by capsaicin-sensitive afferent neurons. It is assumed that endogenous H2S is involved in the regulatory mechanism of acid-induced HCO 3 - secretion and mucosal protection in the duodenum." @default.
- W2027377685 created "2016-06-24" @default.
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- W2027377685 date "2014-05-01" @default.
- W2027377685 modified "2023-09-27" @default.
- W2027377685 title "S6-4 Stimulation of duodenal HCO3− secretion by H2S in rats: Regulatory mechanism and importance in mucosal defense" @default.
- W2027377685 doi "https://doi.org/10.1016/j.niox.2014.03.029" @default.
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