Friström S, Marvola M, Klinge E, Halmekoski J
Acta Pharmacol Toxicol (Copenh). 1977 Feb;40(2):247-58. doi: 10.1111/j.1600-0773.1977.tb02075.x.
The effect of five sympathomimetic amines and some of their acetyl derivatives on the blood pressure of the rat was determined on the left carotid artery. After pretreatment with chlorisondamine (1 mg/kg subcutaneously) the blood pressure rise by sympathomimetic amines and their acetyl derivatives was compared with that of adrenaline. If the potency of adrenaline is specified as 100, the potencies of the other drugs are phenylephrine (metaoxedrinum, NFN) 37, tyramine 1.1, O-acetyltyramine 0.52, amphetamine 0.50, O-diacetylphenylephrine 0.25, ephedrine 0.23, O-acetylephedrine 0.02, N-acetylphenylephrine 0.01. The effects of N-acetyltyramine, N-acetylephedrine and N-acetylamphetamine are even weaker. Reserpine 5.0 or 0.05 mg/kg intraperitoneally 24 hours before the experiment increased the blood pressure rise by the directly acting sympathomimetic amines and their acetyl derivatives, but decreased the effects of the indirectly acting drugs. After treatment with phenoxybenzamine (2 mg/kg intraperitoneally), adrenaline exhibited the greatest blood pressure decrease and the effects of the other drugs in descending order: orciprenaline, O-acetyltyramine, phenylephrine, ephedrine, amphetamine, O-diacetylphenylephrine and O-acetylephedrine. Tyramine did not show any blood pressure decrease. The blood pressure decrease by sympathomimetic amines and by their acetyl derivatives was probably due to beta-receptor stimulation because it was prevented by propranolol. The N-acetyl derivatives recembled their parent drugs with regard to the immediate onset and short duration of their effects. The O-acetyl derivatives exhibited slower onset and longer duration of effect than their parent drugs. Physostigmine-pretreatment diminished the rise in blood pressure by O-acetyltyramine, but the effect of tyramine remained unchanged.
在大鼠左颈动脉上测定了五种拟交感胺及其一些乙酰衍生物对血压的影响。用氯筒箭毒碱（1毫克/千克皮下注射）预处理后，将拟交感胺及其乙酰衍生物引起的血压升高与肾上腺素引起的血压升高进行了比较。如果将肾上腺素的效力规定为100，则其他药物的效力分别为：去氧肾上腺素（甲氧明，NFN）37、酪胺1.1、O - 乙酰酪胺0.52、苯丙胺0.50、O - 二乙酰去氧肾上腺素0.25、麻黄碱0.23、O - 乙酰麻黄碱0.02、N - 乙酰去氧肾上腺素0.01。N - 乙酰酪胺、N - 乙酰麻黄碱和N - 乙酰苯丙胺的作用甚至更弱。实验前24小时腹腔注射5.0或0.05毫克/千克利血平，可增加直接作用的拟交感胺及其乙酰衍生物引起的血压升高，但会降低间接作用药物的效果。用酚苄明（2毫克/千克腹腔注射）处理后，肾上腺素引起的血压下降最大，其他药物的作用按降序排列为：间羟异丙肾上腺素、O - 乙酰酪胺、去氧肾上腺素、麻黄碱、苯丙胺、O - 二乙酰去氧肾上腺素和O - 乙酰麻黄碱。酪胺未表现出任何血压下降。拟交感胺及其乙酰衍生物引起的血压下降可能是由于β受体刺激，因为普萘洛尔可阻止这种下降。N - 乙酰衍生物在作用的即刻起效和持续时间短方面与其母体药物相似。O - 乙酰衍生物的起效比其母体药物慢，作用持续时间更长。毒扁豆碱预处理可减弱O - 乙酰酪胺引起的血压升高，但酪胺的作用保持不变。
