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一氧化氮在兔离体小肠收缩性中的作用:钾离子通道的影响

The role of NO in the contractility of rabbit small intestine in vitro: effect of K+ channels.

作者信息

Grasa L, Rebollar E, Arruebo M P, Plaza M A, Murillo M D

机构信息

Departamento de Farmacología y Fisiología (Fisiología). Facultad de Veterinaria. Universidad de Zaragoza, Zaragoza, Spain.

出版信息

J Physiol Pharmacol. 2005 Sep;56(3):407-19.

PMID:16204763
Abstract

Nitric oxide (NO) is an inhibitory neurotransmitter of intestinal smooth muscle cells. The aim of this study was to determine the role of NO in the contractility of rabbit small intestine smooth muscle in vitro. The amplitude, frequency and tone of spontaneous contractions in longitudinal and circular smooth muscle of duodenum, jejunum and ileum were determined and the sodium nitroprusside (SNP), acetylcholine (ACh) and KCl responses were quantified. L-NAME, L-NNA, L-arginine and D-arginine did not affect the amplitude, frequency and tone of spontaneous contractions. ODQ (10(-6) M) increased the tone of spontaneous contractions of the types of tissues examined, and the amplitude in ileum, without modifying the frequency. SNP (10(-4) M) evoked relaxations that were not influenced by atropine (10(-6) M) plus guanethidine (10(-6) M), apamin (10(-8) M) or glybenclamide (10(-6) M), but were increased by TTX (10(-6) M) and verapamil (10(-7) M). SNP-induced relaxations were reduced by charybdotoxin (10(-8) M) and ODQ (10(-6) M). ODQ (10(-5) M) reduced ACh-induced contractions, but it did not influence KCl-evoked contractions. Those results suggest that NO modulates the spontaneous contractions of small intestine in rabbits. This effect is mediated by cGMP and Ca2+-dependent K+ channels of large conductance.

摘要

一氧化氮(NO)是肠道平滑肌细胞的一种抑制性神经递质。本研究的目的是确定NO在体外对兔小肠平滑肌收缩性的作用。测定十二指肠、空肠和回肠纵行及环行平滑肌的自发收缩幅度、频率和张力,并对硝普钠(SNP)、乙酰胆碱(ACh)和氯化钾(KCl)反应进行定量分析。左旋精氨酸甲酯(L-NAME)、左旋硝基精氨酸甲酯(L-NNA)、左旋精氨酸(L-arginine)和右旋精氨酸(D-arginine)不影响自发收缩的幅度、频率和张力。1H-[1,2,4]恶二唑并[4,3-a]喹喔啉-1-酮(ODQ,10⁻⁶ M)增加了所检测组织类型的自发收缩张力以及回肠的收缩幅度,但不改变频率。SNP(10⁻⁴ M)引起的舒张不受阿托品(10⁻⁶ M)加胍乙啶(10⁻⁶ M)、蜂毒明肽(10⁻⁸ M)或格列本脲(10⁻⁶ M)的影响,但被河豚毒素(TTX,10⁻⁶ M)和维拉帕米(10⁻⁷ M)增强。SNP诱导的舒张被大电导钙依赖性钾通道阻断剂(charybdotoxin,10⁻⁸ M)和ODQ(10⁻⁶ M)减弱。ODQ(10⁻⁵ M)减弱ACh诱导的收缩,但不影响KCl诱发的收缩。这些结果表明NO调节兔小肠的自发收缩。这种作用是由环磷酸鸟苷(cGMP)和大电导钙依赖性钾通道介导的。

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