Department of Hypertension and Diabetology, Medical University of Gdansk, Gdansk, Poland.
J Hypertens. 2011 Mar;29(3):537-41. doi: 10.1097/HJH.0b013e328342b2a9.
Alcohol is associated with acute increases in muscle sympathetic nerve activity (MSNA) in normal individuals. The effects of alcohol on MSNA in patients with hypertension are unknown. Using a randomized, placebo-controlled study design, we tested the hypothesis that there is a differential effect of acute alcohol consumption on cardiovascular function in hypertensive patients compared with normotensive controls.
We examined the effects of oral alcohol intake (1.0 g/kg body weight) and placebo on blood pressure, heart rate, and MSNA in 13 newly diagnosed hypertensive patients and 11 normotensive controls. The two sessions were performed in random order, each study on a separate day.
Baseline MSNA was significantly elevated in the hypertensive patients as compared to the controls (38 ± 2 vs. 28 ± 2 bursts/min; P < 0.01). Placebo had no significant effect on MSNA, blood pressure, or heart rate in either group. In normotensive individuals, alcohol had no significant effect on blood pressure (SBP increased by 1 ± 4 mmHg). By contrast, SBP increased after alcohol in hypertensive patients by 24 ± 6 mmHg (P < 0.001 vs. controls). MSNA increased after alcohol in controls by 83 ± 34% (P < 0.01 vs. baseline). MSNA did not change significantly after alcohol in hypertensive patients (16 ± 7%, not significant), despite a profound blood pressure increase, which would be expected to inhibit sympathetic activity.
Pressor responses to acute alcohol consumption are potentiated in hypertensive patients compared with normotensive controls. Vasoconstrictor sympathetic tone is not suppressed in hypertensive patients after alcohol, despite the enhanced pressor response. Sympathetic neural mechanisms might contribute to both alcohol-related blood pressure increases and cardiovascular events in hypertensive patients.
酒精会导致正常人的肌肉交感神经活动（MSNA）急性增加。酒精对高血压患者 MSNA 的影响尚不清楚。本研究采用随机、安慰剂对照的研究设计，旨在检验以下假设：与正常血压对照者相比，酒精对高血压患者心血管功能的影响存在差异。
我们检测了 13 例新诊断的高血压患者和 11 例正常血压对照者分别口服 1.0 g/kg 体重酒精和安慰剂后血压、心率和 MSNA 的变化。这两种处理方式以随机顺序进行，每项研究在单独的一天进行。
与对照者相比，高血压患者的基础 MSNA 明显升高（38±2 比 28±2 bursts/min；P<0.01）。在两组中，安慰剂对 MSNA、血压或心率均无显著影响。在正常血压对照者中，酒精对血压（收缩压升高 1±4mmHg）没有显著影响。相比之下，高血压患者在饮酒后收缩压升高 24±6mmHg（与对照者比较，P<0.001）。在对照者中，酒精后 MSNA 增加 83±34%（与基础值比较，P<0.01）。然而，高血压患者的 MSNA 没有显著变化（增加 16±7%，无统计学意义），尽管血压明显升高，这会抑制交感神经活动。
与正常血压对照者相比，酒精引起的高血压患者血压升高反应增强。酒精后高血压患者的血管收缩性交感神经张力没有被抑制，尽管血压升高增强。交感神经机制可能导致高血压患者酒精相关的血压升高和心血管事件。
