Recent studies consistently report that acute alcohol consumption increases muscle sympathetic nerve activity (MSNA) in humans. Despite the increased prevalence of hypertension and alcohol consumption in African Americans (AA), no studies have compared MSNA responses to alcohol consumption in AA and Caucasians (C). We hypothesized that alcohol consumption would increase MSNA in both AA and C, but that sympathoexcitatory responses would be augmented in AA. Five minutes of supine heart rate (HR), blood pressure, MSNA, and forearm blood flow were recorded in 8 AA (age, 23±1 yr) and 8 C (age, 22±1 yr) before and 45 min after consumption of 2.5ml of vodka per kg body mass. Increases in blood alcohol content (BAC) were greater in AA (0.105%) compared to C (0.087%; P<0.05). Alcohol elicited similar increases of HR in AA (62±5 to 70±4 beats/min; p<0.001) and C (62±5 to 68±5 beats/min; p<0.001). Contrary to our initial hypothesis, alcohol consumption increased MSNA in C (14±3 to 27±5 bursts/100 heart beats; P<0.05), but did not alter MSNA in AA (28±7 to 29±6 bursts/100 heart beats). Forearm vascular conductance (FVC) was not altered by alcohol consumption in AA or C. However, when sympathetic vascular transduction was calculated (i.e., FVC/MSNA), alcohol consumption reduced sympathetic vascular transduction in C (2.4±0.4 to 1.1±0.2 units; p<0.01), but not AA (1.3±0.4 to 1.3±0.4 units). These findings suggest acute alcohol consumption influences resting MSNA and MSNA‐vascular coupling differently in AA and C, but it is unclear if the different levels of BAC, and perhaps rates of alcohol metabolism, are contributing to these racial differences.
Read full abstract