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戊巴比妥对药物及场电刺激诱导的猫脑动脉和股动脉去甲肾上腺素释放的影响。

Effect of pentobarbital on the noradrenaline release induced by drugs and field electrical stimulation from cerebral and femoral arteries of the cat.

作者信息

Marín J, Recio L

出版信息

Biochem Pharmacol. 1982 Apr 15;31(8):1567-71. doi: 10.1016/0006-2952(82)90381-1.

Abstract

The present studies showed that field electrical stimulation, high potassium (K+), tyramine and ionophore X537A induced tritium release from cerebral and femoral arteries of cat prelabelled with [3H]noradrenaline. The secretion caused by K+ or field stimulation was CA2+-dependent and was antagonized by high concentrations of pentobarbital (10(-4) and 10(-3) M), whereas that induced by the rest of the drugs was unchanged in the same situations. The noradrenaline uptake by these arteries was reduced by pentobarbital (10(-3) M and 10(-4) M). These results suggest that this barbiturate interferes with Ca2+ entry to the adrenergic nerve endings, and therefore antagonizes the noradrenaline release by Ca2+-dependent processes (exocytosis).

摘要

目前的研究表明,电场刺激、高钾(K+)、酪胺和离子载体X537A可诱导预先用[3H]去甲肾上腺素标记的猫脑动脉和股动脉释放氚。K+或电场刺激引起的分泌依赖于Ca2+,并被高浓度的戊巴比妥(10^-4和10^-3 M)拮抗,而其余药物诱导的分泌在相同情况下则无变化。戊巴比妥(10^-3 M和10^-4 M)可降低这些动脉对去甲肾上腺素的摄取。这些结果表明,这种巴比妥酸盐会干扰Ca2+进入肾上腺素能神经末梢,因此拮抗由Ca2+依赖过程(胞吐作用)引起的去甲肾上腺素释放。

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