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一氧化氮合酶抑制剂使豚鼠肠肌间神经丛乙酰胆碱释放增加。

Increase by NO synthase inhibitors of acetylcholine release from guinea-pig myenteric plexus.

作者信息

Kilbinger H, Wolf D

机构信息

Pharmakologisches Institut, Universität Mainz, Germany.

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 1994 May;349(5):543-5. doi: 10.1007/BF00169145.

DOI:10.1007/BF00169145
PMID:7520537
Abstract

The effects of nitric oxide (NO) synthase inhibitors on the electrically evoked release of [3H]acetylcholine were studied in guinea-pig myenteric plexus preparations preincubated with [3H]choline. NG-monomethyl-L-arginine (EC50 5.3 mumol l-1) and NG-nitro-L-arginine (EC50 1.3 mumol l-1) concentration-dependently increased the evoked release of [3H]acetylcholine without affecting the basal outflow. The facilitatory effect of NG-mono-methyl-L-arginine was prevented by L-arginine but not by D-arginine. The results suggest that endogenous NO inhibits the depolarisation-evoked release of acetylcholine.

摘要

在预先用[3H]胆碱孵育的豚鼠肠肌丛制备物中,研究了一氧化氮(NO)合酶抑制剂对电诱发的[3H]乙酰胆碱释放的影响。NG-单甲基-L-精氨酸(EC50 5.3 μmol l-1)和NG-硝基-L-精氨酸(EC50 1.3 μmol l-1)浓度依赖性地增加了[3H]乙酰胆碱的诱发释放,而不影响基础流出量。L-精氨酸可阻止NG-单甲基-L-精氨酸的促进作用,而D-精氨酸则不能。结果表明,内源性NO抑制乙酰胆碱的去极化诱发释放。

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Effects of physostigmine and some nitric oxide-cyclic GMP-related compounds on muscarinic receptor-mediated autoinhibition of hippocampal acetylcholine release.
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Modulation of cholinergic neural bronchoconstriction by endogenous nitric oxide and vasoactive intestinal peptide in human airways in vitro.内源性一氧化氮和血管活性肠肽对人离体气道胆碱能神经介导的支气管收缩的调节作用
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Br J Pharmacol. 1996 Aug;118(8):2073-8. doi: 10.1111/j.1476-5381.1996.tb15646.x.
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Functional evidence for NO-synthase activation by substance P through a mechanism not involving classical tachykinin receptors in guinea-pig ileum in vitro.在豚鼠离体回肠中,P物质通过一种不涉及经典速激肽受体的机制激活一氧化氮合酶的功能证据。
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