Marín J, Recio L
Biochem Pharmacol. 1982 Apr 15;31(8):1567-71. doi: 10.1016/0006-2952(82)90381-1.
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).
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。