Inhibition of noradrenaline release by adenosine.
Inhibition of noradrenaline release by adenosine.
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腺苷抑制去甲肾上腺素的释放。
DOI：
10.1113/jphysiol.1978.sp012446
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发表时间：
1978
期刊：
影响因子：
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通讯作者：
T. Wakade
中科院分区：
文献类型：
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作者：
A. Wakade;T. Wakade
1.腺苷（10（-6）g/ml）可将刺激（5 Hz）预先标记的大鼠输精管诱发的[3 H]去甲肾上腺素释放降低至50%。释放的抑制依赖于腺苷的浓度，并与刺激的频率呈负相关。酚苄明不干扰腺苷的释放作用。2.将预先标记的大鼠输精管暴露于135 mM-K+，释放的[3 H]去甲肾上腺素几乎是暴露于45 mM-K+的10倍。腺苷（10（-6）g/ml）几乎消除了45 mM-K+诱导的释放。但135 mM-K+诱导的细胞凋亡率仅为45%。3.在大鼠唾液腺、心脏和门静脉以及豚鼠心脏和输精管中观察到[3 H]去甲肾上腺素释放抑制。非常高浓度的腺苷（10（-4）g/ml）在兔心脏中减少腺苷的释放（约50%），但猫心脏对腺苷的抑制作用完全不敏感。4.氨茶碱（2 x 10（-4）g/ml.）拮抗腺苷（10（-6）g/ml.）对酚苄明处理的输精管中[3 H]去甲肾上腺素释放的影响。5.四乙基铵（8 x 10（-4）g/ml.）增强刺激诱发的大鼠唾液腺释放几乎十倍。在四乙基铵的存在下，甚至更高的浓度（2 X 10（-5）g/ml.）腺苷未能干扰释放。6.升高外部K+（19 mM）可阻断大鼠输精管中刺激诱发的释放约55%。高K+和腺苷（10（-6）g/ml）的组合，其阻断释放约40%，引起更大的释放抑制（80%）。7.腺苷对刺激诱发的去甲肾上腺素释放的抑制作用的可能作用机制与钙假说有关。
1. Release of [3H]noradrenaline evoked by stimulation (5 Hz) of the pre‐labelled rat vas deferens was reduced to 50% by adenosine (10(‐6) g/ml.). Inhibition of release was dependent on the concentration of adenosine and was inversely related to the frequency of stimulation. Phenoxybenzamine did not interfere with the action of adenosine on release. 2. Exposure of the pre‐labelled rat vas deferens to 135 mM‐K+ released almost 10 times more [3H]noradrenaline than exposure to 45 mM‐K+. Release induced by 45 mM‐K+ was almost abolished by adenosine (10(‐6) g/ml.) but that induced by 135 mM‐K+ was reduced to only 45%. 3. Inhibition of [3H]noradrenaline release was observed in salivary gland, heart and portal vein of the rat, and in the guinea‐pig heart and vas deferens. A very high concentration of adenosine (10(‐4) g/ml.) reduced the release (about 50%) in the rabbit heart, but the cat heart was totally insensitive to the inhibitory action of adenosine. 4. Aminophylline (2 x 10(‐4) g/ml.) antagonized the inhibitory action of adenosine (10(‐6) g/ml.) on the release of [3H]noradrenaline in the phenoxybenzamine‐treated vas deferens. 5. Tetraethylammonium (8 x 10(‐4) g/ml.) enhanced stimulation‐evoked release in the rat salivary gland by almost tenfold. In the presence of tetraethylammonium, even higher concentrations (2 x 10(‐5) g/ml.) of adenosine failed to interfere with release. 6. Elevation of external K+ (19 mM) blocked stimulation‐evoked release in the rat vas deferens by about 55%. Combination of high K+ and adenosine (10(‐6) g/ml.), which blocked release by about 40%, caused still greater inhibition (80%) of the release. 7. The possible mechanism of action of the inhibitory effect of adenosine on the stimulation‐evoked release of noradrenaline is discussed in relation to the calcium hypothesis.