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乙酰胆碱对犬隐静脉中钾离子诱发的去甲肾上腺素释放的抑制作用。

Inhibition by acetylcholine of the norepinephrine release evoked by potassium in canine saphenous veins.

作者信息

Vanhoutee P M, Verbeuren T J

出版信息

Circ Res. 1976 Aug;39(2):263-9. doi: 10.1161/01.res.39.2.263.

DOI:10.1161/01.res.39.2.263
PMID:939012
Abstract

In the dog's saphenous vein acetylcholine inhibits the norepinephrine release caused by nerve stimulation, but not that caused by tyramine. Experiments were performed to determine whether acetylcholine affects the release of norepinephrine evoked by high K+ concentrations. We recorded changes in isometric tension of dog saphenous vein strips. Acetylcholine (5 X 10(-9) to 10(-6) g/ml) caused dose-dependent relaxations during contractions caused by K+ = 40 mEq/liter. These relaxations were not depressed by tetrodotoxin (10(-7) g/ml), which abolished the response to nerve stimulation, but were inhibited by atropine (10(-7) g/ml). Strips of saphenous veins were incubated with [3H]norepinephrine and mounted for superfusion (3 ml/min) and isometric tension recording; the total radioactivity and the amount of intact [3H]norepinephrine present in the superfusate were determined. K+ at 50 mEq/liter increased tension, total radioactivity of the superfusate, and the [3H]norepinephrine afflux; acetylocholine (10(-7) g/ml) depressed the contractions and diminished the efflux of [3H]norepinephrine. Increasing the K+ concentration from 50 to 70 mEq/liter augmented both tension and the evoked release of [3H]norepinephrine. Acetylcholine did not significantly alter the release of [3H]norepinephrine evoked by K+ = 120mEq/liter. These experiments show that acetylcholine inhibits the norepinephrine release evoked by potassium ions, as it does during nerve stimulation. The inhibition of adrenergic neurotransmission is not due to interference with action potential electrogenesis, but probably is caused by hyperpolarization of the adrenergic nerve endings.

摘要

在狗的隐静脉中,乙酰胆碱可抑制神经刺激引起的去甲肾上腺素释放,但不能抑制酪胺引起的去甲肾上腺素释放。进行了实验以确定乙酰胆碱是否影响高钾浓度诱发的去甲肾上腺素释放。我们记录了狗隐静脉条等长张力的变化。在由40 mEq/升钾引起的收缩过程中,乙酰胆碱(5×10⁻⁹至10⁻⁶ g/ml)引起剂量依赖性舒张。这些舒张不受河豚毒素(10⁻⁷ g/ml)的抑制,河豚毒素可消除对神经刺激的反应,但受阿托品(10⁻⁷ g/ml)抑制。将隐静脉条与[³H]去甲肾上腺素一起孵育,然后安装用于灌注(3 ml/分钟)并记录等长张力;测定灌注液中的总放射性和完整[³H]去甲肾上腺素的量。50 mEq/升的钾增加了张力、灌注液的总放射性以及[³H]去甲肾上腺素的内流;乙酰胆碱(10⁻⁷ g/ml)抑制了收缩并减少了[³H]去甲肾上腺素的外流。将钾浓度从50 mEq/升增加到70 mEq/升,增加了张力以及诱发的[³H]去甲肾上腺素释放。乙酰胆碱并未显著改变由120 mEq/升钾诱发的[³H]去甲肾上腺素释放。这些实验表明,乙酰胆碱如同在神经刺激期间一样,抑制钾离子诱发的去甲肾上腺素释放。肾上腺素能神经传递的抑制并非由于对动作电位电发生的干扰,而可能是由肾上腺素能神经末梢的超极化引起的。

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Inhibition by acetylcholine of the norepinephrine release evoked by potassium in canine saphenous veins.乙酰胆碱对犬隐静脉中钾离子诱发的去甲肾上腺素释放的抑制作用。
Circ Res. 1976 Aug;39(2):263-9. doi: 10.1161/01.res.39.2.263.
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