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一氧化氮可诱导豚鼠小肠中乙酰胆碱介导的收缩。

Nitric oxide induces acetylcholine-mediated contractions in the guinea-pig small intestine.

作者信息

Barthó L, Lefebvre R

机构信息

Department of Pharmacology, University Medical School, Pécs, Hungary.

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 1994 Nov;350(5):582-4. doi: 10.1007/BF00173030.

Abstract

In longitudinal muscle/myenteric plexus preparations of the guinea-pig ileum, exogenous nitric oxide (NO) induced concentration-dependent relaxations. In tissues at basal tone, NO (3 x 10(-6) M) induced a moderate relaxation followed by a pronounced contraction, consisting of a quick and sustained component. Tetrodotoxin (5 x 10(-7) M) abolished both phases of the contraction. Atropine (5 x 10(-7) M) abolished the quick component and reduced the sustained component of the contraction; the latter was further suppressed by the selective NK1 receptor antagonist CP 96,345. Hexamethonium (5 x 10(-5) M) failed to affect the contractile response to NO. It is concluded that administration of exogenous NO in the guinea-pig ileum can lead to activation cholinergic and to a lesser degree tachykininergic neurones.

摘要

在豚鼠回肠的纵行肌/肠肌丛标本中,外源性一氧化氮(NO)可引起浓度依赖性舒张。在基础张力状态下的组织中,NO(3×10⁻⁶ M)引起适度舒张,随后是明显的收缩,该收缩由快速和持续成分组成。河豚毒素(5×10⁻⁷ M)消除了收缩的两个阶段。阿托品(5×10⁻⁷ M)消除了收缩的快速成分并减少了收缩的持续成分;后者被选择性NK1受体拮抗剂CP 96,345进一步抑制。六甲铵(5×10⁻⁵ M)未能影响对NO的收缩反应。结论是,在豚鼠回肠中给予外源性NO可导致胆碱能神经元以及程度较轻的速激肽能神经元激活。

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