Rubányi G, Inovay J
Acta Physiol Acad Sci Hung. 1982;59(2):181-6.
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.
研究了低浓度(1 - 10微摩尔)镍(Ni2+)对离体大鼠门静脉制备物自发收缩活性的影响。为区分突触前和突触后作用,比较了Ni2+诱导的电场刺激(80V/5 cm;1毫秒;1 - 32赫兹)或外源性去甲肾上腺素(NE)引起的等长力发展变化。Ni2+抑制自发等长力发展,降低基础张力,但显著增加收缩频率。实验结果表明,与抑制外源性去甲肾上腺素引起的收缩相比,选择性刺激肾上腺素能神经的作用受到的抑制更为明显,这表明除了突触后作用外,Ni2+还影响该血管制备物中的突触前机制(即NE释放)。