Gastric HCO3- secretion induced by mucosal acidification:: different mechanisms depending on acid concentration
Gastric HCO3- secretion induced by mucosal acidification:: different mechanisms depending on acid concentration
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DOI：
10.1163/156856005774423836
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发表时间：
2005-01-01
影响因子：
5.8
通讯作者：
Takeuchi, Koji
中科院分区：
文献类型：
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作者：
Aihara, Eitaro;Hayashi, Masamune;Takeuchi, Koji
我们比较了在不同的盐酸浓度（100和200 mM盐酸）在大鼠胃粘膜酸化诱导的HCO3分泌反应。在氨基甲酸乙酯麻醉下，将胃固定在离体室上，并在奥美拉唑（60 mg/kg，i.p.）抑制酸分泌的情况下用盐水灌注。在pH 7.0下使用pH-稳态法并通过加入2mM HCl测量HCO3-分泌。通过暴露于100 mM或200 mM HCl的粘膜进行酸化10 min。在100和200 mM HCl的粘膜酸化增加了HCO3-的分泌，最大HCO3-响应是后者浓度的1.5倍。由100和200 mM HCl诱导的HCO3-反应都完全抑制由先前管理的吲哚美辛，前列腺素（PG）生产的抑制剂。200 mM HCl的HCO3刺激作用也显着衰减预处理与N-G-硝基L-精氨酸甲酯（L-NAME），一氧化氮（NO）合酶的抑制剂，以及辣椒素敏感的传入神经元的化学消融，而100 mM HCl的影响，这些治疗。我们的结论是，粘膜酸化刺激胃HCO3-分泌在不同的机制，取决于酸的浓度;由100 mM盐酸引起的反应是由PG介导的，而由200 mM盐酸引起的辣椒素敏感的传入神经元和NO介导的，除了PG。
We compared the HCO3- secretory responses induced by mucosal acidification at different HCl concentrations (100 and 200 mM HCl) in the rat stomach. Under urethane anesthesia, the stomach was mounted on an ex vivo chamber and perfused with saline under inhibition of acid secretion by omeprazole (60 mg/kg, i.p.). The HCO3- secretion was measured at pH 7.0 using a pH-stat method and by adding 2 mM HCl. The acidification was performed by exposure of the mucosa to 100 mm or 200 mM HCl for 10 min. The secretion of HCO3- was increased by acidification of the mucosa at both 100 and 200 mM of HCl, and the maximal HCO3- response was 1.5-times greater at the latter concentration. The HCO3- responses induced by 100 and 200 mM HCl were both totally inhibited by prior administration of indomethacin, an inhibitor of prostaglandin (PG) production. The HCO3- stimulatory effect of 200 mM HCl was also significantly attenuated by pre-treatment with N-G-nitro L-arginine methyl ester (L-NAME), the inhibitor of nitric oxide (NO) synthase, as well as chemical ablation of capsaicin-sensitive afferent neurons, whereas that of 100 mM HCl was affected by neither of these treatments. We conclude that the mucosal acidification stimulates gastric HCO3- secretion in different mechanisms, depending on the concentration of acid; the response caused by 100 mM HCl is mediated only by PGs, while that caused by 200 mM HCl is mediated by both capsaicin-sensitive afferent neurons and NO, in addition to PGs.