Lee S S, Kim H, Park Y C, Song J H, Lee M H, Chung E S, Lee S J, Imm C W
Korean J Intern Med. 1987 Jul;2(2):214-20. doi: 10.3904/kjim.1987.2.2.214.
To assess the contribution of sympathetic outflow to blood pressure in patients with essential hypertension, clonidine induced variations of plasma norepinephrine, mean arterial pressure and the pulse rate three hours after a 300 μg dose of oral clonidine, an antihypertensive agent that decreases central sympathetic outflow, were studied. Baseline and clonidine suppressed plasma norepinephrine levels were not significantly different between the normal controls and patients with essential hypertension. The average plasma norepinephrine level, mean arterial pressure and pulse rate were significantly decreased from the baseline value in both normal control and essential hypertension (p<.005). The depressor response to sympathetic inhibition after clonidine were exaggerated in significant proportion in patients with essential hypertension compared to normal control group. Our study suggests that the pressor sensitivity to norepinephrine plays more important role than sympathetic overactivity in some patients with essential hypertension.
为评估交感神经流出对原发性高血压患者血压的影响，研究了口服300μg可乐定（一种可降低中枢交感神经流出的抗高血压药物）3小时后，可乐定诱导的血浆去甲肾上腺素、平均动脉压和脉搏率的变化。正常对照组和原发性高血压患者的基线血浆去甲肾上腺素水平以及可乐定抑制后的血浆去甲肾上腺素水平无显著差异。正常对照组和原发性高血压患者的平均血浆去甲肾上腺素水平、平均动脉压和脉搏率均较基线值显著降低（p<0.005）。与正常对照组相比，原发性高血压患者中相当比例的人对可乐定后交感神经抑制的降压反应增强。我们的研究表明，在一些原发性高血压患者中，对去甲肾上腺素的升压敏感性比交感神经过度活跃起更重要的作用。
