Floras J S, Aylward P E, Mark A L, Abboud F M
Department of Internal Medicine, University of Iowa College of Medicine, Iowa City.
J Hypertens. 1990 May;8(5):443-8. doi: 10.1097/00004872-199005000-00008.
Adrenaline facilitates the neural release of endogenous noradrenaline by stimulating prejunctional beta-receptors on adrenergic nerve endings. Recently, we demonstrated the functional significance of this action in the control of vascular resistance in young subjects with normal blood pressure. In the present study, we tested the hypothesis that the effects of adrenaline on neurogenic vasoconstriction are exaggerated in humans with borderline hypertension. Forearm blood flow was measured simultaneously in the experimental and contralateral arms of seven young men with borderline hypertension. We compared forearm vasoconstrictor responses to a reflex stimulus to noradrenaline release (lower-body negative pressure, LBNP) and to intra-arterial infusion of noradrenaline before and 30 min after brachial artery infusion of adrenaline (50 ng/min). These doses had no systemic effects. In the experimental arm, the vasoconstrictor response to LBNP was 65% greater 30 min after the adrenaline infusion (P = 0.075), whereas the response to intra-arterial noradrenaline decreased by 36% (P greater than 0.1). Forearm vascular responses to LBNP in the contralateral control arm that did not receive adrenaline were similar before and after the adrenaline infusion. The ratio of forearm vasoconstrictor responses (i.e. the increase in forearm vascular resistance) with LBNP to the forearm vasoconstrictor response to noradrenaline in the experimental arm was used as an index of neural release of the neurotransmitter noradrenaline. This ratio increased from 0.8 to 2.1 (P less than 0.05) after the adrenaline infusion. These facilitatory neural after-effects of adrenaline were similar in magnitude to our previous observation in young normotensive subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
肾上腺素通过刺激肾上腺素能神经末梢的节前β受体促进内源性去甲肾上腺素的神经释放。最近，我们证明了这一作用在控制血压正常的年轻受试者血管阻力中的功能意义。在本研究中，我们检验了以下假设：在临界高血压患者中，肾上腺素对神经源性血管收缩的作用会被夸大。对7名临界高血压青年男性的实验侧和对侧手臂同时测量前臂血流量。我们比较了在肱动脉输注肾上腺素（50 ng/min）前及输注后30分钟，前臂对去甲肾上腺素释放的反射刺激（下体负压，LBNP）和动脉内输注去甲肾上腺素的血管收缩反应。这些剂量无全身效应。在实验侧手臂，肾上腺素输注后30分钟，对LBNP的血管收缩反应增加了65%（P = 0.075），而对动脉内去甲肾上腺素的反应降低了36%（P大于0.1）。未接受肾上腺素的对侧对照臂中，对LBNP的前臂血管反应在肾上腺素输注前后相似。实验侧手臂中，将对LBNP的前臂血管收缩反应（即前臂血管阻力增加）与对去甲肾上腺素的前臂血管收缩反应之比用作神经递质去甲肾上腺素神经释放的指标。肾上腺素输注后，该比值从0.8增至2.1（P小于0.05）。肾上腺素的这些促进性神经后效应在程度上与我们之前在血压正常的年轻受试者中的观察结果相似。（摘要截短于250字）
