Distinct mechanisms of acid-induced HCO-3 secretion in normal and slightly permeable stomachs
Distinct mechanisms of acid-induced HCO-3 secretion in normal and slightly permeable stomachs
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DOI：
10.1152/ajpgi.00048.2006
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发表时间：
2006-09-01
影响因子：
4.5
通讯作者：
Takeuchi, Koji
中科院分区：
文献类型：
--
作者：
Aihara, Eitaro;Sasaki, Yoko;Takeuchi, Koji
我们研究了酸诱导的HCO 3-分泌的调节机制，在轻微渗透性大鼠胃暴露于高渗NaCl后。在氨基甲酸乙酯麻醉下，将大鼠胃固定在一个腔室上，并用盐水灌注，并使用pH-stat方法和通过加入2 mM HCl在pH 7.0下测量HCO 3-的分泌。酸化的正常胃与100 mM盐酸增加HCO 3-分泌，这种反应完全抑制预处理消炎痛，但不NG-硝基-L-精氨酸甲酯（L-NAME）或化学消融的辣椒素敏感的传入神经元。暴露于0.5 M NaCl的胃扰乱了未搅拌的粘液凝胶层，而不损害表面上皮细胞。胃对0.5 M NaCl的反应是以吲哚美辛可降解的方式分泌稍多的HCO 3-，对10 mM HCl的反应是HCO 3-分泌显著增加，尽管10 mM HCl在正常胃中没有影响。酸诱导的HCO 3-反应在NaCl处理的胃显着，但部分衰减消炎痛，L-NAME，或感觉传入阻滞，并完全取消时，这些治疗相结合。这些结果表明，胃HCO 3-分泌响应酸是由两个独立的机制，一个介导的前列腺素（PGs）和其他的感觉神经元和一氧化氮（NO）。正常胃中酸诱导的HCO（-）（3）分泌完全由内源性PG介导，但当胃对酸具有轻微渗透性时，感觉神经元和NO显著促进了该反应。
We investigated the regulatory mechanism of acid-induced HCO3- secretion in the slightly permeable rat stomach after an exposure to hyperosmolar NaCl. Under urethane anesthesia, a rat stomach was mounted on a chamber and perfused with saline, and the secretion of HCO3- was measured at pH 7.0 using a pH-stat method and by adding 2 mM HCl. Acidification of the normal stomach with 100 mM HCl increased HCO3- secretion, and this response was totally inhibited by pretreatment with indomethacin but not NG-nitro-L-arginine methyl ester (L-NAME) or chemical ablation of capsaicin-sensitive afferent neurons. Exposure of the stomach to 0.5 M NaCl deranged the unstirred mucus gel layer without damaging the surface epithelial cells. The stomach responded to 0.5 M NaCl by secreting slightly more HCO3-, in an indomethacin-inhibitable manner, and responded to even 10 mM HCl with a marked rise in HCO3- secretion, although 10 mM HCl did not have an effect in the normal stomach. The acid-induced HCO3- response in the NaCl-treated stomach was significantly but partially attenuated by indomethacin, L-NAME, or sensory deafferentation and was totally abolished when these treatments were combined. These results suggest that gastric HCO3- secretion in response to acid is regulated by two independent mechanisms, one mediated by prostaglandins (PGs) and the other by sensory neurons and nitric oxide ( NO). The acid-induced HCO (-)(3) secretion in the normal stomach is totally mediated by endogenous PGs, but, when the stomach is made slightly permeable to acid, the response is markedly facilitated by sensory neurons and NO.