Kooner J S, Peart S, Mathias C J
Medical Unit, St Mary's Hospital and Medical School, London, UK.
J Hypertens Suppl. 1988 Dec;6(4):S544-6. doi: 10.1097/00004872-198812040-00171.
The role of central pressor mechanisms in the maintenance of blood pressure in six hypertensive patients with angiographically proven unilateral renal artery stenosis was investigated by studying the haemodynamic and hormonal responses before and after central sympathetic blockade with clonidine. To assess the dependency of blood pressure on the direct effects of angiotensin II, the same patients were studied on a separate occasion after administration of the angiotensin converting enzyme (ACE) inhibitor, captopril. There was a substantial fall in blood pressure after administration of clonidine with a smaller fall after captopril. Clonidine-induced hypotension was accompanied by a fall in cardiac output, through a reduction in the stroke volume and heart rate. Forearm vascular resistance was unchanged. There was a selective decrease in digital skin vascular resistance and plasma noradrenaline, indicating reduced sympathetic activity. Plasma renin activity and aldosterone levels did not fall. After administration of captopril, there was a fall in cardiac output due to a fall in the stroke volume but not in the heart rate. Forearm vascular resistance, digital skin vascular resistance and plasma noradrenaline were unchanged. Plasma renin activity rose and plasma aldosterone fell. We conclude that in our hypertensive patients with renal artery stenosis, clonidine lowered blood pressure by a reduction in central sympathetic activity independently of renin suppression. In these patients captopril had minimal hypotensive effects, indicating a smaller role for the direct vascular effects of angiotensin II.
通过研究可乐定进行中枢交感神经阻滞前后的血流动力学和激素反应，探讨了中枢升压机制在6例经血管造影证实为单侧肾动脉狭窄的高血压患者维持血压中的作用。为了评估血压对血管紧张素II直接作用的依赖性，在另一个时间点对同一组患者给予血管紧张素转换酶（ACE）抑制剂卡托普利后进行了研究。服用可乐定后血压大幅下降，服用卡托普利后血压下降幅度较小。可乐定引起的低血压伴随着心输出量的下降，这是通过每搏输出量和心率的降低实现的。前臂血管阻力未改变。手指皮肤血管阻力和血浆去甲肾上腺素选择性降低，表明交感神经活动减弱。血浆肾素活性和醛固酮水平未下降。服用卡托普利后，由于每搏输出量下降而非心率下降，心输出量降低。前臂血管阻力、手指皮肤血管阻力和血浆去甲肾上腺素未改变。血浆肾素活性升高，血浆醛固酮降低。我们得出结论，在我们的肾动脉狭窄高血压患者中，可乐定通过降低中枢交感神经活动来降低血压，与肾素抑制无关。在这些患者中，卡托普利的降压作用极小，表明血管紧张素II的直接血管作用较小。
