Abstract-To investigate whether sodium sensitivity of blood pressure participates in the relationship of arterial hypertension to chronic alcohol consumption, 30 alcoholics detoxified from 6 to 12 months and 30 teetotaler controls underwent a dietary sodium manipulation study. They received a daily 55 mmol sodium diet for 7 days, followed by a 260 mmol sodium diet for 7 days. Changes in 24-hour urinary sodium excretion between the end of each period were similar in alcoholics and controls (202Ϯ16 SEM mmol and 227Ϯ11, respectively). Plasma renin activity in alcoholics was lower than in controls at both low (2.4Ϯ0.4 ng angiotensin I/mLϫh -1 versus 3.7Ϯ0.2, PϽ0.003) and high sodium intake (0.47Ϯ0.10 versus 0.82Ϯ0.10, PϽ0.05), with smaller variations in alcoholics (Ϫ1.9Ϯ0.3 versus Ϫ2.9Ϯ0.2, PϽ0.009). In alcoholics, alteration in sodium intake was followed by greater changes in both systolic and mean blood pressure (ambulatory blood pressure monitoring), which rose by 10.6Ϯ2.2 mm Hg and 7.3Ϯ1.5 versus 4.7Ϯ1.4 and 3.9Ϯ1.0 in controls, respectively (PϽ0.03 for systolic and PϽ0.05 for mean blood pressure). The ratio of changes in mean blood pressure to those in 24-hour urinary sodium excretion was higher in alcoholics (0.044Ϯ 0.011 mm Hgϫmmol Ϫ1 versus 0.018Ϯ0.0041, PϽ0.005). Our data show that in detoxified alcoholics, there is an abnormal response of both blood pressure and plasma renin activity to variations in salt intake similar to that in sodium-sensitive arterial hypertension. The precise relationship between the sodium sensitivity of blood pressure in detoxified alcoholics and the long-term influence of alcohol on blood pressure remains to be elucidated. Key Words: alcoholism Ⅲ blood pressure Ⅲ sodium sensitivity A n association between chronic exposure to alcoholic beverages and elevation in blood pressure (BP) has been widely recognized. 1Ϫ6 Cross-sectional and epidemiological reports have indicated that chronic consumption of alcohol equal to 3 drinks per day or more may be an independent variable that acts on BP (in addition to obesity, Na intake, smoking, physical activity, age, gender, and race), with a magnitude similar to that observed for obesity and even greater than that of Na intake by itself. 2,3,5 Studies in moderate drinkers and chronic alcoholics have also shown a relationship between current alcohol intake and BP, 6 -10 although no further increase in BP was detected over a daily alcohol intake of 6 drinks per day. 2,4,10 Furthermore, prospective studies have indicated that alcohol consumption was accompanied by increasing BP over time and by an elevated risk of developing clinical arterial hypertension (HTN). 1,4,5,11 Finally, intervention studies in alcoholics have almost invariably shown a significant decrease in BP with reduced or no alcohol exposure. 12Ϫ16 Several investigations on the mechanisms that underlie the link between chronic alcohol consumption and HTN have been conducted involving, as the candidate abnormalities genetic predisposition, 10 hyperdynamic circulation with high cardia...