The mechanism underlying stimulation of gastric HCO3− secretion by the nitric oxide synthase inhibitor Ng‐nitro‐l‐arginine methyl ester in rats
The mechanism underlying stimulation of gastric HCO3− secretion by the nitric oxide synthase inhibitor Ng‐nitro‐l‐arginine methyl ester in rats
复制标题
一氧化氮合酶抑制剂 Ng-硝基-L-精氨酸甲酯刺激大鼠胃 HCO3− 分泌的机制
DOI：
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发表时间：
1994
影响因子：
4.1
通讯作者：
S. Okabe
中科院分区：
文献类型：
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作者：
K. Takeuchi;T. Ohuchi;M. Tachibana;S. Okabe
摘要：我们研究了一氧化氮（NO）合成酶抑制剂Ng‐硝基‐1‐精氨酸甲酯（l‐Name）刺激麻醉大鼠胃HCO3−分泌的机制。将大鼠胃置于离体室中，灌注生理盐水，在没有酸分泌的情况下（奥美拉唑预处理）测量HCO3−的分泌。静脉给药l‐Name（1‐5 mg/kg）会增加胃HCO3−分泌剂量，并伴有动脉血压升高和心率降低，同时给药l‐精氨酸（200 mg/kg）可拮抗这些作用。迷走神经切断术不影响血压升高的反应，但显著抑制l‐Name引起的心率下降和HCO3−分泌增加。育亨宾（5mg /kg s.c）或哌唑嗪（0.5 mg/kg s.c）预处理也能抑制l‐Name的HCO3−刺激作用。这些药物单独引起血压下降，并降低l - Name引起的血压反应的幅度，从而抑制心率变化。当l‐Name引起的HCO3−输出的变化与不同条件下血压的变化（从基础值开始）相对应时，发现这两个参数之间存在显著的关系。这些结果表明，l‐Name刺激胃HCO3−分泌与抑制内源性NO的产生有关，这一机制可能部分是由l‐Name的压力反应引起的迷走传出神经反射介导的。
Abstract We investigated the mechanism underlying stimulation of gastric HCO3− secretion by the nitric oxide (NO) synthase inhibitor Ng‐nitro‐l‐arginine methyl ester (l‐Name) in anaesthetized rats. A rat stomach was mounted in an ex vivo chamber, superfused with saline, and HCO3− secretion was measured in the absence of acid secretion (omeprazole pretreatment). Intravenous administration of l‐Name (1‐5 mg/kg) increased gastric HCO3− secretion dose dependently with concomitant rise in arterial blood pressure and decrease in heart rate, and these effects were all antagonized by simultaneous administration of l‐arginine (200 mg/kg). Vagotomy did not affect the increased blood pressure response but significantly inhibited the decrease in heart rate and increase of HCO3− secretion caused by l‐Name. The HCO3− stimulatory action of l‐Name was also inhibited by pretreatment with either yohimbine (5 mg/kg s.c.) or prazosin (0.5 mg/kg s.c.). These agents alone caused a decrease in blood pressure, and reduced the magnitude of blood pressure response caused by l‐Name, leading to inhibition of heart rate changes. When the change in HCO3− output induced by l‐Name was plotted against the change in blood pressure (from basal values) under various conditions, a significant relationship was found between these two parameters. These results suggest that l‐Name stimulates gastric HCO3− secretion in association with the inhibition of endogenous NO production, and this mechanism may be in part mediated by a neural reflex through vagal efferent nerves, resulting from the pressor response to l‐Name.