Glick G, Wechsler A S, Epstein S E
J Clin Invest. 1968 Mar;47(3):511-20. doi: 10.1172/JCI105747.
The mechanisms of reflex vasodilation were studied in an innervated canine hindlimb preparation which was perfused at a constant rate. Reflex vasodilation was produced by suddenly increasing the pressure in the trunk by the intravenous injection of norepinephrine, with consequent stimulation of the baroreceptors. When the basal vasoconstrictor tone exerted by the sympathetic nervous system on the systemic arterial bed was minimized, either by pretreatment with the alpha adrenergic blocking agent phenoxybenzamine or with reserpine, which depletes endogenous catecholamine stores, reflex vasodilation was virtually abolished. Administration of cocaine, a drug which blocks reuptake of norepinephrine by the nerve terminals, significantly reduced reflex vasodilation, the response after cocaine averaging 47% of the vasodilator response in the control period. Cocaine also potentiated the vasoconstriction caused by intra-arterially administered norepinephrine but attenuated the vasoconstriction induced by tyramine. The antihistamine, tripelennamine, had effects similar to those of cocaine. It is suggested, therefore, that reflex vasodilation results from a sudden decrease in the level of norepinephrine at the neuroeffector junction, which is a consequence of the cessation of norepinephrine secretion, together with continued and possibly augmented uptake. When the uptake mechanism is impaired, either by the administration of cocaine or tripelennamine, the magnitude of reflex vasodilation is diminished. It does not appear necessary to postulate active secretion of a vasodilator substance to account for reflex vasodilation.
在以恒定速率灌注的有神经支配的犬后肢标本中研究了反射性血管舒张的机制。通过静脉注射去甲肾上腺素突然升高躯干压力，从而刺激压力感受器，产生反射性血管舒张。当交感神经系统对全身动脉床施加的基础血管收缩张力通过用α肾上腺素能阻断剂苯氧苄胺预处理或用耗竭内源性儿茶酚胺储备的利血平预处理而减至最小时，反射性血管舒张实际上被消除。给予可卡因（一种阻断神经末梢去甲肾上腺素再摄取的药物）可显著降低反射性血管舒张，可卡因给药后的反应平均为对照期血管舒张反应的47%。可卡因还增强了动脉内注射去甲肾上腺素引起的血管收缩，但减弱了酪胺诱导的血管收缩。抗组胺药曲吡那敏具有与可卡因相似的作用。因此，有人提出反射性血管舒张是由于神经效应器连接处去甲肾上腺素水平突然降低所致，这是去甲肾上腺素分泌停止以及持续且可能增强的摄取的结果。当摄取机制受损时，无论是通过给予可卡因还是曲吡那敏，反射性血管舒张的幅度都会减小。似乎没有必要假设一种血管舒张物质的主动分泌来解释反射性血管舒张。
