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肾上腺素对调节兔离体主动脉刺激诱发的3H-去甲肾上腺素释放的肾上腺素能受体的突触前作用。

Presynaptic action of adrenaline on adrenoceptors modulating stimulation-evoked 3H-noradrenaline release from rabbit isolated aorta.

作者信息

Abrahamsen J, Nedergaard O A

机构信息

Department of Pharmacology, School of Medicine, Odense University, Denmark.

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 1989 Mar;339(3):281-7. doi: 10.1007/BF00173578.

DOI:10.1007/BF00173578
PMID:2566930
Abstract

The purpose of this investigation was to study the effect of adrenaline on presynaptic adrenoceptors by recording the release of 3H-noradrenaline evoked by electrical-field stimulation. Adrenaline (10(-10)-3 x 10(-9) mol/l) had no effect on the 3H-overflow evoked by stimulation of aorta preloaded with 3H-noradrenaline. At 10(-8) and 3 x 10(-8) mol/l, the 3H-overflow was decreased by up to 47%. The maximum decrease was more marked in the presence of either cocaine (3 x 10(-5) mol/l) plus corticosterone (4 x 10(-5) mol/l), cocaine (3.3 x 10(-6) mol/l) plus normetanephrine (4 x 10(-5) mol/l), or desipramine (10(-6) mol/l) plus normetanephrine (10(-5) mol/l). The relationship between adrenaline-induced decrease and stimulation-frequency was dependent on the experimental design: either the decrease was the same at all frequencies (1-16 Hz) or it was more marked, the lower the frequency (1 greater than 3 greater than 8 Hz). Phentolamine and rauwolscine (both 10(-6) mol/l) antagonized the inhibitory effect of adrenaline (10(-8)-10(-6) mol/l). Phenoxybenzamine (10(-6) mol/l), prevented the inhibitory effect. No enhancing effect of adrenaline (10(-9)-10(-6) mol/l) was observed in the presence of these three alpha-adrenoceptor antagonists. Our results suggest that adrenaline activates inhibitory alpha 2-adrenoceptors, but not facilitatory beta-adrenoceptors on postganglionic sympathetic nerve terminals in rabbit aorta.

摘要

本研究的目的是通过记录电场刺激诱发的3H-去甲肾上腺素释放,来研究肾上腺素对突触前肾上腺素能受体的作用。肾上腺素(10(-10)-3×10(-9)mol/L)对预加载3H-去甲肾上腺素的主动脉刺激诱发的3H溢出无影响。在10(-8)和3×10(-8)mol/L时,3H溢出最多可降低47%。在存在可卡因(3×10(-5)mol/L)加皮质酮(4×10(-5)mol/L)、可卡因(3.3×10(-6)mol/L)加去甲变肾上腺素(4×10(-5)mol/L)或地昔帕明(10(-6)mol/L)加去甲变肾上腺素(10(-5)mol/L)的情况下,最大降幅更明显。肾上腺素诱导的降低与刺激频率之间的关系取决于实验设计:要么在所有频率(1-16Hz)下降低程度相同,要么频率越低(1>3>8Hz)降低越明显。酚妥拉明和萝芙木碱(均为10(-6)mol/L)拮抗肾上腺素(10(-8)-10(-6)mol/L)的抑制作用。酚苄明(10(-6)mol/L)可防止这种抑制作用。在这三种α-肾上腺素能受体拮抗剂存在的情况下,未观察到肾上腺素(10(-9)-10(-6)mol/L)的增强作用。我们的结果表明,肾上腺素激活兔主动脉节后交感神经末梢上的抑制性α2-肾上腺素能受体,但不激活促进性β-肾上腺素能受体。

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本文引用的文献

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Modulation of noradrenaline release through activation of presynaptic beta-adrenoreceptors.通过激活突触前β-肾上腺素能受体来调节去甲肾上腺素释放。
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