镍离子对大鼠离体门静脉自发、电和去甲肾上腺素刺激的等距收缩的影响。

G Rubányi, J Inovay
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引用次数: 0

摘要

研究了低浓度(1 ~ 10微米)镍(Ni2+)对离体大鼠门静脉制剂自发收缩活性的影响。为了区分突触前和突触后的作用,我们分别用电场刺激(80V/5 cm;1微秒;1-32 Hz)或外源性去甲肾上腺素(NE)。Ni2+抑制自发等长力发展,降低基底张力,但显著增加收缩频率。实验发现,Ni2+对肾上腺素能神经选择性刺激的抑制作用比外源性去甲肾上腺素引起的收缩抑制作用明显,这表明除了突触后作用外,Ni2+还影响该血管制备中的突触前机制(即ne -释放)。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effect of nickel ions on spontaneous, electrically and norepinephrine stimulated isometric contractions in the isolated portal vein of the rat.

The effect of low concentrations (1-10 microM) of nickel (Ni2+) was studied on the spontaneous contractile activity of isolated rat portal vein preparations. To distinguish between presynaptic and postsynaptic actions, Ni2+-induced changes of isometric force development evoked either by electrical field stimulation (80V/5 cm; 1 msec; 1-32 Hz) or by exogenous norepinephrine (NE) were compared. Ni2+ inhibited spontaneous isometric force development, decreased basal tone but significantly increased the frequency of contractions. The experimental findings that inhibition of the effect of selective stimulation of adrenergic nerves was significantly more pronounced than the depression of contractions evoked by exogenous norepinephrine indicate that in addition to postsynaptic actions, Ni2+ influences presynaptic mechanisms (i.e. NE-release) in this vessel preparation.

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