Potentiated sympathetic and hemodynamic responses to alcohol in hypertensive vs. normotensive individuals

Abstract

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.