一氧化氮合酶抑制剂对麻醉大鼠十二指肠碱性分泌的影响。

Effects of nitric oxide synthase inhibitors on duodenal alkaline secretion in anesthetized rats.

作者信息

Takeuchi K, Ohuchi T, Miyake H, Niki S, Okabe S

机构信息

Department of Applied Pharmacology, Kyoto Pharmaceutical University, Japan.

出版信息

Eur J Pharmacol. 1993 Jan 26;231(1):135-8. doi: 10.1016/0014-2999(93)90694-d.

DOI:10.1016/0014-2999(93)90694-d

PMID:7680316

Abstract

We examined the effects of NG-nitro-L-arginine methyl ester (L-NAME), the nitric oxide (NO) synthase inhibitor, on duodenal HCO3- secretion in anesthetized rats. L-NAME (1-5 mg/kg i.v.), given as a single injection, increased HCO3- secretion in a dose-dependent manner. This effect of L-NAME was mimicked by NG-monomethyl-L-arginine (50 mg/kg i.v.) and was significantly antagonized by the simultaneous administration of L-arginine (200 mg/kg i.v.) but not D-arginine. The increased HCO3- response to L-NAME was also significantly reduced in vagotomized animals. These findings suggest that the inhibition of NO biosynthesis leads to an increase of duodenal HCO3- secretion, partly mediated by the vagus nerves.

摘要

我们研究了一氧化氮（NO）合酶抑制剂NG-硝基-L-精氨酸甲酯（L-NAME）对麻醉大鼠十二指肠HCO₃⁻分泌的影响。单次静脉注射L-NAME（1-5mg/kg）可剂量依赖性地增加HCO₃⁻分泌。NG-单甲基-L-精氨酸（50mg/kg静脉注射）可模拟L-NAME的这种作用，同时静脉注射L-精氨酸（200mg/kg）可显著拮抗该作用，而D-精氨酸则无此作用。在迷走神经切断的动物中，L-NAME引起的HCO₃⁻反应增加也显著降低。这些发现表明，抑制NO生物合成会导致十二指肠HCO₃⁻分泌增加，部分是由迷走神经介导的。