Acute alcohol consumption is reported to decrease mean arterial pressure (MAP) during orthostatic challenge, a response that may contribute to alcohol-mediated syncope. Muscle sympathetic nerve activity (MSNA) increases during orthostatic stress to help maintain MAP, yet the effects of alcohol on MSNA responses during orthostatic stress have not been determined. We hypothesized that alcohol ingestion would blunt arterial blood pressure and MSNA responses to lower body negative pressure (LBNP). MAP, MSNA, and heart rate (HR) were recorded during progressive LBNP (−5, −10, −15, −20, −30, and −40 mmHg; 3 min/stage) in 30 subjects (age 24 ± 1 yr). After an initial progressive LBNP (pretreatment), subjects consumed either alcohol (0.8 g ethanol/kg body mass; n = 15) or placebo ( n = 15), and progressive LBNP was repeated (posttreatment). Alcohol increased resting HR (59 ± 2 to 65 ± 2 beats/min, P < 0.05), MSNA (13 ± 3 to 19 ± 4 bursts/min, P < 0.05), and MSNA burst latency (1,313 ± 16 to 1,350 ± 17 ms, P < 0.05) compared with placebo (group × treatment interactions, P < 0.05). During progressive LBNP, a pronounced decrease in MAP was observed after alcohol but not placebo (group × time × treatment, P < 0.05). In contrast, MSNA and HR increased during all LBNP protocols, but there were no differences between trials or groups. However, alcohol altered MSNA burst latency response to progressive LBNP. In conclusion, the lack of MSNA adjustment to a larger drop in arterial blood pressure during progressive LBNP, coupled with altered sympathetic burst latency responses, suggests that alcohol blunts MSNA responses to orthostatic stress.

Acute alcohol consumption has been reported to decrease mean arterial pressure (MAP) during orthostatic challenge, a response that may contribute to alcohol‐mediated syncope. Muscle sympathetic nerve activity (MSNA) increases during orthostatic stress to help maintain MAP, yet the influence of alcohol on MSNA during orthostatic stress has not been determined. We hypothesize that alcohol ingestion will blunt MSNA responses to lower body negative pressure (LBNP). MAP, MSNA, and heart rate (HR) were recorded during progressive LBNP (−5, −10, −15, −20, −30, and −40 mmHg; 3 min/stage) in 22 subjects (age 25 ± 1 yrs). After a baseline progressive LBNP (Trial 1), subjects were randomly assigned to either the placebo (n=11) or alcohol (n=11) group and repeated the progressive LBNP (Trial 2). Resting MAP increased (P<0.05) similarly with placebo (83 ± 2 to 88 ± 2 mmHg) and alcohol (82 ± 2 to 87 ± 3 mmHg). Resting HR (60 ± 2 to 64 ± 2 beats/min) and MSNA (15 ± 4 to 24 ± 4 bursts/min) increased (P<0.05) with alcohol, but not placebo. A significant time × condition × group interaction (P<0.05) was observed for MAP, demonstrating a more pronounced decrease in MAP during progressive LBNP with alcohol. MSNA and HR increased during all LBNP protocols, but there were no differences between trials or groups. In conclusion, alcohol decreases MAP responses to orthostatic stress, but these decreases do not appear to be mediated by MSNA. Supported by NIH.

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