(Hypertension. 2000;35:869.)
© 2000 American Heart Association, Inc.
Scientific Contributions |
Sodium Sensitivity of Blood Pressure in Long-Term Detoxified Alcoholics
From the Center For Study and Treatment of Alcoholism, Dipartimento di Medicina Interna e Scienze Biomediche, and Istituto di Patologia Speciale Medica (A.M.), University of Parma, Italy.
Correspondence to Cristiana Di Gennaro, MD, Centro di Alcologia, Dipartimento di Medicina Interna e Scienze Biomediche, Via Gramsci 14, I-43100 Parma, Italy. E-mail panorama{at}ipruniv.cce.unipr.it
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Abstract |
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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 (202±16 SEM mmol and 227±11, respectively). Plasma renin activity in alcoholics was lower than in controls at both low (2.4±0.4 ng angiotensin I/mLxh-1 versus 3.7±0.2, P<0.003) and high sodium intake (0.47±0.10 versus 0.82±0.10, P<0.05), with smaller variations in alcoholics (-1.9±0.3 versus -2.9±0.2, P<0.009). 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 10.6±2.2 mm Hg and 7.3±1.5 versus 4.7±1.4 and 3.9±1.0 in controls, respectively (P<0.03 for systolic and P<0.05 for mean blood pressure). The ratio of changes in mean blood pressure to those in 24-hour urinary sodium excretion was higher in alcoholics (0.044± 0.011 mm Hgxmmol-1 versus 0.018±0.0041, P<0.005). 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 • blood pressure • sodium sensitivity
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Introduction |
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An association between chronic exposure to alcoholic beverages and elevation in blood pressure (BP) has been widely recognized.1 6 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 7 8 9 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.12 16 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 cardiac output,17 18 the activated renin-angiotensin-aldosterone system,19 20 and the sympathetic nervous system17 18 or of its central regulation.17 However, the precise nature of this relationship remains to be elucidated. This uncertainty derives in part from the complexity of potential interactions of alcohol with BP regulation. These latter studies include acute or subacute circulatory and neurohormonal responses to very recent alcohol load12 13 17 18 or to early alcohol withdrawal,21 23 both conditions potentially associated with sympathetic nervous system activation and wide alterations in fluid and electrolyte balance. These mechanisms, which are not different from those in acute alcohol intoxication17 18 24 or binge drinking25 in nonalcoholic subjects and largely independent of the chronic effects on BP of alcohol by itself, may have played a confounding role in studies in active or early withdrawing alcoholics. Recent studies26 however showed that BP levels of medium-term detoxified alcoholics, although almost completely returned into the normotensive range, are related to lifetime total alcohol consumption and duration of alcoholism. In addition, King et al27 observed in such patients an abnormal hypertensive in response to the isometric handgrip that was related to the levels of alcohol consumption.28 Finally, an impaired endothelium-dependent vasorelaxation was found at 3 months in abstaining chronic alcoholics.29 These findings would collectively indicate that some mechanisms of BP dysregulation secondary to previous alcohol exposure are operating even after medium-term alcohol detoxification. Our preliminary observations in long-term (6 to 12 months) detoxified alcoholics30 showed a unexpected prevalence of low to normal plasma renin activity (PRA). Because a trend toward lowered baseline PRA and impaired responsiveness to Na restriction are often associated with sodium-sensitive essential HTN,31 32 the hypothesis could be advanced that sodium-sensitivity contributes to the linkage between previous chronic alcohol exposure and BP levels. Thus, we studied BP and PRA responses to dietary Na manipulation in a group of long-term detoxified alcoholics and in a comparable control group of nonalcoholics. The results presented here show a marked salt sensitivity of BP in long-term detoxified alcoholics.
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Methods |
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Subjects
Thirty alcoholic patients attending the Center for Study and Treatment of Alcoholism at the University of Parma participated in the study. Diagnosis of chronic alcoholism had been made during an in-hospital examination, including assessment of drinking history and severity of alcohol dependency.33 34 After an in-hospital detoxification, alcoholics had been involved in the rehabilitation program Alcoholics-in-Treatment Clubs (Clubs degli Alcolisti in Trattamento, ATC). This self-help, multifamily, community-based, therapeutic approach includes educational and relational dynamic groups.35 In this program, volunteer experts who work in voluntary or public health institutions help to involve the patients and their families in ATC. Alcoholic patients were compared with 30 teetotaler control subjects (10 females, 20 males) among volunteer personnel working in ATCs (n=10, 2 females, 8 males) and wives (n=6), husbands (n=6), sisters (n=2), or brothers (n=6) of alcoholics. Because these individuals were all involved in ATC activities, they were carefully interrogated on even moderate past alcohol consumption. Lifelong alcohol-free subjects only were admitted to the study. No subject had clinical evidence of psychiatric illness, took any medication, or had a history of drug abuse other than alcoholism. Any cause of secondary HTN was excluded. For alcoholics, detoxified state had been assessed carefully for 6 to 12 months before the study by weekly physical examination, interrogation, and determinations of blood and urine alcohol, serum
-glutamyltranspeptidase, and red cell
mean volume.
Study Protocol
The study, in conformity with ethical guidelines of our
Institution, was performed on a day-hospital basis after informed
consent was obtained by each subject. During a 4-week, run-in phase,
subjects underwent clinic BP measurements on 3 separate occasions, 
5
days apart. On the last of these visits, 24-hour urinary sodium
excretion (UNaV) and recumbent PRA were measured
at the habitual Na intake. Subjects were considered hypertensive when
the mean value of 3 measured SBPs was 160 mm Hg or that of DBP
was 95 mm Hg or both. The responses to dietary Na manipulation
were assessed by comparing BP measurement on the seventh day of a
low-Na intake period (55 mmol Na per day) with that of the seventh
day of the subsequent period at a high Na intake (260 mmol Na per
day). To obtain the target Na intake, subjects were instructed to
adhere to a basic diet designed by the hospital dietitian and adjusted
to each subject’s caloric intake, which provided 55 mmol Na,
65 mmol K, 20 mmol calcium, and 3 mmol Mg during both
phases of the study. Diets were provided in a detailed written form.
Everyday subjects completed daily a food questionnaire, which was
examined in our alcohol unit. During the high Na period, the basic diet
was supplemented with an addition 205 mmol Na per day, which was
dispensed daily by us in small paper sachets that each contained 1
g NaCl (or 17 mmol Na). At the seventh day of each period, 24-hour
urine was collected for Na and creatinine
(UCreatV) excretion measurement, blood was drawn
for recumbent PRA and plasma creatinine, and BP
measurements with 24-hour ambulatory blood pressure monitoring (ABPM)
were performed. Study subjects were specifically instructed to maintain
their smoking habits and coffee intake as well as their physical and
work activities.
BP Measurement
Twenty-four–hour ABPM was performed concomitantly with 24-hour
urine collection from the morning of day 6 to that of day 7 of each
dietary period with an automated, noninvasive oscillometric device (TM
2421, A&D Co) that was attached to the upper, nondominant arm. BP was
registered at 15-minute intervals from 7 AM to 10
PM and 30-minute intervals at nighttime.
Biochemical Measurements
Urinary Na was measured by spectrophotometry and
creatinine by routine clinical methods. PRA was measured by
radioimmunoassay with the Renin Maya Kit (Biodata; lowest detection
limit of 0.039 ng/mL, percent variation coefficient 4 to 6) and
expressed as ng · mL-1 ·
h-1 of angiotensin I.
Calculations and Assessment of Salt Sensitivity of BP and
Statistical Analysis
From each ABPM record, mean values for SBP, DBP, and MBP
were obtained. To assess the relationship of BP changes to those in Na
intake (and excretion), the sodium sensitivity index
(SSI)36 was calculated in each subject as the ratio of
change in MBP (
MBP) to that in UNaV
(UNaV) from low to high Na period and
expressed as mm Hgxmmol-1. Simple linear
regression analysis was used to detect any relationship of SSI
to BMI, age, UNaV at baseline, and at both low
and high Na intake. In each group, subjects were also divided into
salt-sensitive and salt-resistant groups according to 6
different, discriminating criteria. First, as suggested by de La Sierra
et al,37 records obtained in each subject from ABPM in
either low or high Na periods were individually analyzed and
compared statistically. The Student’s t test or
nonparametric Mann-Whitney U test was used as appropriate.
Subjects who showed significant changes (P<0.05 or less) in
MBP between low and high Na periods were considered salt sensitive. The
other 5 criteria were based on the choice of different changes in MBP
from low to high Na intake as the cutoff point to define an individual
as salt sensitive. These values were 10
mm Hg,38 5 mm Hg,39 10% of
low Na value,36 and 5% of low Na value,40
respectively. Finally, changes in MBP between 5 and 10 mm Hg
indicated an intermediate response (undetermined), with >10
mm Hg change for salt sensitivity and <5 mm Hg for salt
resistance.32 Mean values were compared by Student’s
t test or Mann-Whitney U test with correction for ties as
appropriate. 
2 analysis with Yates
correction for continuity or the Fisher exact probability test, when
necessary, was performed to compare the prevalence of salt sensitivity
and salt resistance among the groups of alcoholics and controls or
their subgroups, which was obtained by dividing each of them into
hypertensive or normotensive subjects according to baseline BP. Data
are expressed as mean±SEM. SPSS 8.0 software was used for statistical
calculations.
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Results |
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Table 1 summarizes the demographic and clinical characteristics of alcoholic and control subjects. No statistical differences were found for age, BMI, gender distribution, and smoking habit between the 2 groups. Table 2 represents baseline BP, UNaV, and PRA in alcoholic and control subjects. There were no significant differences for both BP values and prevalence of HTN between the groups. Baseline UNaV was slightly but significantly higher in alcoholics. PRA was substantially lower in alcoholics than in nonalcoholic subjects. In Table 3, we summarize the effects of dietary Na manipulation. Values of UNaV at the end of both low and high Na periods were slightly lower in alcoholics than in controls. Changes in UNaV, however, were essentially the same in both groups. In addition, variations in UNaV in reference to creatinine were very close, as was the small, but significant increase in creatinine excretion and clearance at high Na intake. These findings indicate a satisfactory compliance for fixed Na intake and a good comparability of the 2 groups. PRA in alcoholics was lower than in controls under both conditions of stimulation (low Na) and suppression (high Na). In addition, changes in PRA after alteration of Na intake were markedly blunted in alcoholics. The shift from a low-Na to high-Na diet produced significant changes in SBP, DBP, and MBP in both groups. These variations however were much more pronounced in alcoholics for both SBP and MBP, which increased by 10.6 mm Hg (8.7%) and 7.3 (8.2%) in alcoholics and by 4.7 mm Hg (3.8%) and 3.9 (4.4%) in controls, respectively. SSI was more than 2x higher in alcoholics than in controls as represented in Figure 1. SSI values ranged from -0.144 to +0.210 mm Hgxmmol-1 in alcoholics and from -0.014 to +0.068 in controls. Several subjects in both groups had a SSI value <0, ie, a fall instead of a rise in BP after shifting from low to high Na intake. This may not only be an expression of the well-known counterregulation of BP in response to alteration in Na intake,31 32 but it may also contribute to the wide variability of SSI values. Linear regression analysis showed that SSI was not related to BMI (r=0.096, NS), age (r=0.231, NS), baseline UNaV (r=0.01, NS), or UNaV at both low and high Na intake (r=-0.125, NS, and -0.0035, NS, respectively). Table 4 shows the distribution of salt-sensitive and salt-resistant subjects within each group, on the basis of several proposed discriminating criteria. Data indicate a prevalence of salt-sensitivity in alcoholics that is significantly higher than that in nonalcoholics, according to 5 of the 6 criteria adopted to define an individual as salt sensitive or salt resistant. When both alcoholics and controls were divided into a normotensive or a hypertensive subgroup, 6 of 20 normotensive controls and 4 of 10 hypertensive controls were salt sensitive on the basis of ABPM criteria (P=0.27).37 Nine of 11 hypertensive alcoholics and 13 of 19 normotensive alcoholics were salt sensitive (P=0.25). Salt sensitivity was more prevalent (13 of 19) in normotensive alcoholics than in normotensive controls (6 of 20,
2=4.3, P<0.05), as it was
in hypertensive alcoholics versus hypertensive controls (9 of 11 and 4
of 10, respectively), although without reaching a statistical
significance (P=0.056). The difference in SSI between
normotensive alcoholic and normotensive control subgroups was also
significant (0.043± 0.018 mm Hgxmmol-1
and 0.013±0.005, respectively, P=0.032).
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Discussion |
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The relationship between alcohol and HTN is firmly established by now.1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 In spite of continuing interest in the underlying mechanisms of hypertension, its physiological basis still remains elusive.10 The main purpose of the present study was to investigate whether the salt sensitivity of BP is involved in the alcohol/HTN relationship. The role of Na intake in alcohol-related HTN has been previously described by Parker et al,41 who were unable to find any further BP fall by adding moderate, short-term Na restriction to alcohol reduction in drug-treated hypertensive drinkers. This single negative report however may be well explained by an overwhelming depressor effect of lowered alcohol intake that is able to obscure, but not rule out, any role of other mechanisms. Hence, provided the possible impact of acute or subacute changes, secondary to recent alcohol load or withdrawal and essentially independent of chronic actions of alcohol by itself, alcoholic patients detoxified from 6 to 12 months would allow us to circumvent such potential confounding factors. On the other hand, studies in detoxified alcoholics,26 27 28 29 showed that there may be a residual effect of long-term alcohol consumption on BP regulation, focusing on total lifetime alcohol consumption26 34 as the marker of total cumulative alcohol exposure. In medium-term detoxified patients, York and Hirsh26 demonstrated that BP is related to both duration of alcohol career and total estimated lifetime alcohol intake, suggesting that cardiovascular susceptibility to alcohol toxicity may reflect both lifetime alcohol load and length of drinking career. These considerations convinced us that long-term detoxified, pharmacologically untreated heavy alcoholic people is an acceptable clinical setting to study any chronic mechanism linking alcohol consumption and susceptibility to HTN. The main finding we show here is that long-term detoxified chronic alcoholics, when compared with teetotallers, display more significant changes in BP in response to those in dietary Na intake and Na excretion. The ratio between
MBP and UNaV (SSI) was much higher than
that measured in control subjects. In addition, a wider prevalence of
salt sensitivity was apparent in alcoholics, on the basis of all but
one of criteria used to discriminate between salt sensitivity and salt
resistance. The findings obtained by comparing hypertensive and
normotensive subgroups showed no difference in the prevalence of salt
sensitivity between normotension and HTN in both alcoholics and
nonalcoholics, whereas salt sensitivity seemed to be more prevalent in
alcoholics than in nonalcoholics irrespective of baseline BP levels.
This might confirm that previous alcoholism is a determinant of salt
sensitivity of BP at any given level of baseline BP. Both baseline PRA
and its responsiveness to dietary Na manipulation were markedly blunted
in detoxified alcoholics in comparison with controls. This is at
variance to some previous anecdotal suggestions19 20 of
participation of an activated
renin-angiotensin-aldosterone system in HTN of
alcoholics. Instead of consistent elevations in PRA, more
accurate studies showed a trend to a fall in PRA from high-normal
levels toward suppressed values in short- to medium-term withdrawing
alcoholics,21 22 23 42 43 44 a finding that may be related to
the recovery from a previous dehydrated state.23 43 44
Abnormal changes of both BP and PRA to alteration in Na intake, such as
those observed in alcoholics, are typically associated with salt
sensitivity in essential HTN.31 32 Thus, salt sensitivity
of BP could contribute to the relationship of BP levels to the previous
alcohol consumption in detoxified alcoholics,26 although
the nature of this association cannot be explained by the present
study. Individuals with salt-sensitive essential hypertension and
chronic alcoholism show other similarities such as a hyperactivity of
the sympathetic nervous system,17 18 31 32 45 46 an
insulin–resistant state with
hyperinsulinemia,31 32 46 47 and an
impaired endothelium-dependent
vasorelaxation,29 48 which is detectable even after
abstaining from alcohol for 3 months. In addition, salt sensitivity in
essential HTN seems to be an independent risk factor for the
development of cardiovascular and renal
complications.31 32 46 48 Taken together, these findings
should indicate salt sensitivity of BP as a candidate abnormality that
contributes to the susceptibility of alcohol abusers to
cardiovascular diseases.10 On the other
hand, a precise linkage between the present findings, which were
obtained in the particular clinical setting of detoxified, heavy
alcoholics, and the alcohol/HTN relationship in more moderate drinkers
cannot be established at this time. Additional studies on the salt
sensitivity of BP in less severe alcoholics or on the effects of
drinking in salt-sensitive or salt-resistant hypertensive
subjects is necessary. In conclusion, the present study shows that
in long-term detoxified, heavy alcoholics, there is an abnormal
response of both BP and RAAS to Na intake similar to that observed in
salt-sensitive hypertensives. Further studies are needed on the role of
salt sensitivity of BP in the alcohol/HTN relationship in the general
population.
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Acknowledgments |
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This work was supported by grants from the University of Parma. The authors thank Maria Angela Ziveri, PhD, for measurements of plasma renin activity.
Received October 18, 1999; first decision November 11, 1999; accepted November 22, 1999.
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