Donate Help Contact The AHA Sign In Home
American Heart Association
Hypertension
Search: search_blue_button Advanced Search
Hypertension. 1996;28:133-138

This Article
Right arrow Abstract Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by York, J. L.
Right arrow Articles by Hirsch, J. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by York, J. L.
Right arrow Articles by Hirsch, J. A.

(Hypertension. 1996;28:133-138.)
© 1996 American Heart Association, Inc.


Articles

Residual Pressor Effects of Chronic Alcohol in Detoxified Alcoholics

James L. York; Judith Ann Hirsch

the Research Institute on Addictions, Buffalo, and Department of Physiology, State University of New York at Buffalo.

Correspondence to James L. York, PhD, Research Institute on Addictions, 1021 Main St, Buffalo, NY 14203.


*    Abstract
up arrowTop
*Abstract
down arrowIntroduction
down arrowMethods
down arrowResults
down arrowDiscussion
down arrowReferences
 
Although research in population studies has indicated that recent alcohol intake is positively correlated with blood pressure, there is a need to study the relationship of blood pressure to measures of lifetime alcohol intake in alcoholics. To this end, we assessed systolic and diastolic pressures and lifetime alcohol intake through structured interviews with 253 normotensive recovering alcoholics. Blood pressures were first corrected with multiple linear regression for the influence of confounding or modifying variables and then were regressed against alcohol consumption measures. Systolic pressure was significantly correlated (positively) with only a few measures of recent alcohol intake, and the correlations were not high (r2=.05 to .11, P<.05). Diastolic pressure was found to be highly and positively correlated with the duration of the drinking career, but more so in blacks than in whites. The total lifetime dose of alcohol was found to be positively correlated with diastolic but not systolic pressure, but only in black male alcoholics. The steeper slope of the regression of blood pressure versus lifetime total alcohol or duration of the drinking career in black alcoholics suggests greater cardiovascular susceptibility to alcohol toxicity as lifetime doses increase and as the drinking career lengthens.


Key Words: alcohol • blood pressure • epidemiology • ethnic groups • gender


*    Introduction
up arrowTop
up arrowAbstract
*Introduction
down arrowMethods
down arrowResults
down arrowDiscussion
down arrowReferences
 
The risk of death from stroke increases continuously with systolic blood pressures (SBPs) greater than 112 mm Hg or diastolic blood pressures (DBPs) greater than 78 mm Hg in men, with blacks being more at risk than whites.1 Findings such as these emphasize the importance of studying factors, such as alcohol intake, that are associated with increases in blood pressure (BP).2 3 Although numerous empirical and epidemiological studies have suggested a positive association between BP and recent alcohol consumption in moderate drinkers, there is still considerable controversy over the exact relationships that exist between current or past alcohol intake, SBP or DBP, and modifying or confounding variables such as age, sex, race, adiposity, smoking, and physical activity.4 5 6 7

Still missing is a study of the relationship of BP to alcohol consumption using lifetime alcohol intake as a drinking measure in a cohort of alcoholic subjects. In studies of the "residual" toxic effects of long-term alcohol use in alcoholics, our laboratory has focused on total lifetime alcohol consumption as an important variable that reflects the total cumulative exposure to the alcohol toxin over the drinking career.8 9 10 This thinking has been guided by the assumption that the probability of tissue or organ system alterations should increase as a function of the cumulative dose.

We undertook the current study to determine whether a relationship exists between the total lifetime dose of alcohol and current BP in normotensive detoxified alcoholics. The study was also motivated by the now-acknowledged need to develop more precise measures of ethanol exposure in individuals7 as well as lifetime total exposure estimates.5 11 To this end, the dilution of ethanol into body water, rather than body weight, was used, and detailed drinking histories that began with the earliest drinking phase were compiled.


*    Methods
up arrowTop
up arrowAbstract
up arrowIntroduction
*Methods
down arrowResults
down arrowDiscussion
down arrowReferences
 
Subjects
Research protocols were approved by a human subjects review board, and informed consent was obtained from all subjects. A racially mixed cohort of 253 alcoholic subjects (187 men, 66 women) between the ages of 20 and 59 years were recruited from local alcoholism treatment centers and were screened for polydrug abuse and/or major medical problems, including hypertension. An average of 35 days elapsed between the discontinuation of drinking and the testing described here. The maintenance of abstinence was a condition for participation and was verified by questioning and breath alcohol tests when subjects reported for testing at the Research Institute on Addictions. More details regarding subject selection can be found elsewhere.12 13

Physical Measures
Height and weight (Physicians Healthometer Scale) were determined shortly after subjects reported to the laboratory. Seated heart rate and BP measurements were made with an oscillometric digital sphygmomanometer (Takeda Medical, average of three readings) 15 to 20 minutes after the subject reported for testing. Subjects with BPs exceeding 95 mm Hg DBP or 160 mm Hg SBP were not allowed to participate. Total body water was determined by bioelectric impedance methodology,14 15 which also provided an estimate of percent body fat.

Assessment of Lifestyle Characteristics and Drinking History
Subjects accepted into the study were given or mailed questionnaires to complete before reporting to the laboratory for an interview and BP assessment. The questionnaires provided information regarding subject characteristics that might be confounding or modifying variables with regard to BP. For instance, the level of physical activity (exercise) typically expended in work, leisure, and sport activities was assessed with a 16-item self-administered form.16 The Health and Daily Living Questionnaire17 was used to characterize subjects with regard to major medical problems. An index of socioeconomic status was calculated for each subject from information on occupation and formal education with the Hollingshead and Redlich "two-factor" index of social position.18 The Alcohol Dependency Scale19 was used to obtain information regarding the severity of alcohol dependency, as reflected in psychological, physical, or social dysfunction during the 12 months preceding testing.

Because alcoholics are typically exposed to large amounts of alcohol over a period of many years, it was considered of paramount importance to obtain accurate estimations of alcohol intake beginning with the onset of regular drinking. To this end, detailed lifetime alcohol consumption histories were assessed by means of a structured interview.13 20 Quantity, frequency, and type of beverage, as well as the influence of life events on drinking behavior, were recorded for each succeeding phase of the subjects' drinking career, beginning with the period in their life at which they first began drinking at least one drink per month. A "phase" was defined as a period of time during which alcohol drinking habits remained relatively constant. Data from individual phases were summed to obtain lifetime drinking measures. The duration of the drinking career was defined as the number of years elapsing since regular drinking (at least once per month) began. The interview also provided measures of alcohol consumption for the current drinking phase of each subject. Thus, measures of recent alcohol intake similar to those commonly used in epidemiological studies were also obtained. The availability of total body water measures on all subjects in the current study allowed us to express alcohol intake in terms of the acknowledged volume of distribution for alcohol12 21 22 rather than total body weight, which is often used as a denominator. Thus, a measure theoretically more related to the "biologically effective" dose of ethanol was obtained.

Statistical Analyses
Multiple linear regressions were first performed to generate predicted BP values after removal of the variance contributed by the possible confounders of age, activity, medical status, body mass index, smoking, or socioeconomic status. This was accomplished with the Number Cruncher statistical package (V.5.01, Jerry Hintze, Kaysville, Utah). The robust regression option was used, in which all covariates were equally weighted. Separate and independent analyses were performed on each of the four subgroups of Table 1Down. Corrected BP values were then regressed against alcohol consumption measures.


View this table:
[in this window]
[in a new window]
 
Table 1. Demographic, Lifestyle, and Alcohol Intake Characteristics of Alcoholics


*    Results
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowMethods
*Results
down arrowDiscussion
down arrowReferences
 
Subject Characteristics
Alcoholics in all four subgroups registered scores on the Alcohol Dependency Scale that were indicative of a substantial level of alcohol dependence, with physical dependence likely (scores in excess of 22).20 These subjects were of low socioeconomic status (Table 1Up), owing primarily to their recruitment from local inner-city (Buffalo) public alcoholism treatment programs. The low representation of women in the treatment programs is reflected in the small number of women in this study. The white and black subgroups within each sex were quite similar in terms of physical and lifestyle characteristics (Table 1Up). Reports of medical problems (health score) were low for all subgroups, owing to the screening out of subjects with major medical problems. Mean BPs were normal for all four of the subgroups.

Alcohol Intake in Alcoholics
Reported alcohol intake was similar for white and black subgroups within each sex for both lifetime and recent drinking (Table 1Up). Sex differences in alcohol intake are discussed in detail elsewhere.12 Note that alcohol intake is reported for both drinking days (days during which drinking took place) and as a daily average value, as if the alcohol consumed in a week were spread equally over the 7 days of the week.

Values reported for recent drinking refer to the drinking phase that immediately preceded entry into treatment. Drinking day consumption for the recent phase is in excess of the drinking day values averaged over the drinking career (lifetime drinking), reflecting the progressive increase in alcohol intake with succeeding drinking phases in alcoholics.13

Relationship of Alcohol Intake to BP
BPs were first corrected for the influence of confounding or modifying variables (age, activity, body mass index, health score, socioeconomic status, cigarettes per day) before regression against alcohol consumption measures. The only covariates that were significantly correlated with BP were age (for DBP in black men [r2=.17, P<.001] and SBP in black women [r2=.30, P<.05]) and body mass index (for DBP in black men [r2=.06, P<.05] and SBP in white men [r2=.09, P<.001] and black women [r2=.28, P<.05]).

Table 2Down lists the lifetime drinking measures that were significantly correlated with DBP after correction for the covariates. Not found to be significantly correlated with either SBP or DBP were lifetime measures of daily averages or drinking day averages. In women, the duration of drinking was the only drinking measure that was significantly correlated with DBP. The only group to display a significant relationship of SBP to any lifetime drinking measure was black women, with regard to duration of drinking (y=89.5+0.902 [0.271 SE]x; r2=.338, P<.01).


View this table:
[in this window]
[in a new window]
 
Table 2. Lifetime Drinking Measures Significantly Correlated With Diastolic Pressure in Alcoholics

Some recent phase drinking measures were significantly correlated with SBP (but not DBP), but the correlations were quite small: Drinking day average and daily average, both expressed in grams ethanol per kilogram body water, were significantly correlated in white men (for both measures, r2=.05, P<.05); frequency of drinking (recent phase) was significantly correlated in black men (r2=.05, P<.05); and maximum ethanol in grams ethanol per kilogram body water was significantly correlated in white women (r2=.11, P<.05).

The strongest associations were with the duration of drinking measure and in black men. Race effects in the same direction were also observed in women. The scatterplots in the FigureDown illustrate that the slope of the relationship between DBP and duration of drinking was steeper in blacks than in whites (P<.02 for men, P<.01 in women; t tests for slopes), indicating a greater effect of increases in duration of drinking on DBP in blacks. Those regressions (FigureDown) were corrected (in addition to the covariates previously mentioned) for the influence of lifetime total alcohol. The slopes were quite shallow for the relationship of DBP to lifetime total dose or lifetime total number of drinks (Table 2Up).



View larger version (24K):
[in this window]
[in a new window]
 
Figure 1. Relationship of duration of alcohol consumption to diastolic pressure in alcoholics. Linear regression analyses were performed on blood pressure values corrected for the influence of age, activity, socioeconomic status, body mass index, health score, cigarettes per day, and lifetime total alcohol. Standard errors for the slopes are included in the equations in parentheses.


*    Discussion
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowMethods
up arrowResults
*Discussion
down arrowReferences
 
The findings of the present study clearly suggest that there may be residual pressor effects of prior chronic alcohol exposure in alcoholics and that blacks may be more affected as lifetime doses increase or as the duration of the drinking career increases. Although blacks are generally considered to be at greater risk for hypertension than whites,23 24 most previous research has indicated that blacks are no more responsive than whites to the pressor effects of alcohol when general population samples are studied.6 An exception was the report of a continuous relationship of more drinking to higher DBP (but not SBP) in a nonalcoholic population of black men.25 Our findings on black men are somewhat in harmony with the above report and suggest that black alcoholics may run a greater risk than white alcoholics for BP elevations after long-term consumption of large doses of alcohol.

The finding that duration of alcohol exposure was significantly correlated with DBP independent of the amount of alcohol consumed (lifetime total alcohol) in alcoholics was surprising because it suggests that the amount of alcohol consumed is not of paramount importance. This would seem to contradict our basic notions of dose-response relationships in toxicology. However, it may be possible that each alcoholic is titrating his/her alcohol intake at a personal maximal level in accordance with his/her own personal sensitivity to alcohol, such that all subjects (within sexes) are in effect receiving somewhat similar "biologically toxic" doses. Under such circumstances, the length of exposure to the toxin would become the factor that contributes predominantly to the magnitude of the insult.26

Methodological Considerations and Limitations
To our knowledge this is the first study to relate BP to alcohol intake measures expressed in terms of individually estimated tissue exposure levels in subjects (ie, dilution of ingested ethanol into the body water compartment). This measure would seem to be, in the absence of actual blood concentration measurements, the most reflective of tissue exposures to ethanol.12 21 22 Of course, noticeably lacking from this measure (and other common measures, for that matter) is a consideration of the rate of alcohol ingestion (eg, drinks per hour and resultant blood alcohol concentrations) and of alcohol disappearance (metabolism). Notwithstanding these limitations, we were surprised to find the measure of lifetime total alcohol in terms of grams of ethanol per kilogram of total body water not to be more highly correlated with BP than the measure of lifetime total in terms of the simple number of drinks consumed. However, the only significant correlation of recent drinking measures with BP (SBP only) were observed with measures of alcohol intake in terms of body water dilution.

Because epidemiological studies such as this rely on statistical associations, they lack the ability to directly address cause-and-effect relationships among variables. Moreover, although such studies attempt to control for the influence of potentially confounding variables, this is not always possible. For instance, because alcohol has caloric value, heavy consumers often reduce their intake of other caloric sources that contribute to balanced nutrition. Thus, it is quite possible that the duration of poor or compromised nutrition coincides with the duration of the drinking career. In the present study, we can only assert that subjects had been exposed to adequate diets at treatment facilities for several weeks before participation in this study, at least ensuring that acute electrolyte or nutritional imbalances were not present at the time BPs were measured.

Threshold and Ceiling Effects
Previous studies have consistently found a positive relationship between recent daily alcohol intake and BP in nonalcoholic subjects, with some evidence for a threshold for pressor effects at three or more drinks per day or per drinking day.4 5 6 Because of the significant period of abstinence for the alcoholic subjects of the present study, perhaps it is not surprising that the correlations of recent alcohol intake with BP were few and not very large. However, the finding of residual pressor effects even after a mean of 35 days of abstinence also may not be surprising, considering that these alcoholics had been consuming alcohol at the rate of 12 to 16 drinks per day, 3 to 4 days per week, for a duration of 19 to 25 years (Table 1Up).

Another suggestion from previous studies has been that of a possible "ceiling" effect at around 9 drinks per day, above which further hypertensive effects of alcohol are not observed.25 27 The alcoholics of the current study usually exceeded the value of 9 drinks per day (mean, 17 to 23 drinks per day; Table 1Up). Moreover, the increase in DBP with increases in the duration of drinking and lifetime dose suggests that the ceiling may be higher than previously suggested and/or that the ceiling may not be as obvious when other drinking dimensions, such as lifetime dose or duration of the drinking career, are used. Needless to say, the findings of the current study must be considered to apply only to normotensive alcoholic populations. Alcoholics with clinical hypertension may represent a select group of susceptible individuals who display heightened, or at least different, relationships of BP to alcohol consumption practices than do the subjects of the present study. Past studies have demonstrated that such hypertensive alcoholics usually experience a rapid and significant drop of BP with abstinence.28 29

Short-term Versus Long-term Models
Considering that a single lifetime alcohol interview may require 20 to 60 minutes to administer in alcoholics, it is not surprising that the relationship of BP to alcohol consumption has not previously been examined with the lifetime total dose measure of alcohol exposure. However, because alcohol consumption patterns may escalate considerably over the drinking career in alcoholics, current alcohol intake cannot be considered to be representative of past intake.13 The sparse and low correlations of BP to alcohol intake during the most recent drinking phase in alcoholics illustrate the utility of the measure of total lifetime alcohol consumption. It is noteworthy that significant relationships between lifetime total dose of alcohol and skeletal and cardiac muscle impairment have also been demonstrated.30 31 Further study will be required for determination of whether the relationships are truly causal or whether the lifetime total exposure measures reflect the operation of perhaps a third lifestyle factor related to both excessive chronic alcohol intake and cardiovascular status.

Researchers now recognize neurohumoral, central nervous system, and local direct effects as possible mechanisms by which alcohol exposure may bring about changes in cardiovascular function. Various models have been presented.4 5 6 29 However, because much of the research into the pressor effects of alcohol consumption has measured BP within the course of weekly alcohol consumption habits in nonalcoholic or general population samples, the findings pertain somewhat more to short-term pressor effects of alcohol, although longer-term alcohol-induced alterations may have been superimposed on the shorter-term actions. Interpretations must acknowledge that the physiological basis of short-term pressor effects of alcohol are distinct from the long-term effects that may represent cumulative toxicities requiring long periods of abstinence for recovery.32 33 34 The findings from the present study are unique owing to the focus on alcoholic populations, the requirement of abstinence for a period of weeks before testing, and the inclusion of a lifetime measure of alcohol consumption.

There are probably also "intermediate-term" hypertensive effects that decline a few days after alcohol consumption is discontinued in moderate drinkers32 35 and in alcoholics.28 Thus, studies that measure BP during the course of recent daily or weekly alcohol consumption may be measuring the combined effects of recent (short- or intermediate-term) alcohol intake superimposed on longer-term perturbations that are more permanent or require longer periods of time for recovery. Moreover, short-term abstinence from alcohol in physically-dependent alcoholics or heavy drinkers may superimpose additional cardiovascular perturbations on any long-lasting toxic effects. We are not aware of any "long-term" models that might explain in physiological terms the mechanisms by which residual actions of prolonged alcohol exposure may influence cardiovascular status. Because alcohol intake patterns may have extended for some time into the past, it cannot be ascertained to what extent any relationships between alcohol and BP are "intermediate term" or even "longer term" in most studies. The observations on alcoholics reported here indicate that there is still some "dysregulation" of BP related to lifetime alcohol dose even after a mean of 35 days of abstinence. Interestingly, another recent study has revealed BP dysregulations persisting for 3 to 4 weeks of abstinence in transitory hypertensive alcoholics whose BP had returned to normal.36 Disentanglement of the complex interplay of immediate, short-term, or longer-term pressor effects of alcohol is needed to refine this area of epidemiology.


*    Acknowledgments
 
This work was supported by grant RO1-6867 from the National Institute on Alcoholism and Alcohol Abuse. The authors gratefully acknowledge the cooperation of officials at Alcoholism Services of Erie County, BryLin Hospital, Clearview Treatment Services, The City Mission, Stutzman Alcoholism Treatment Center, Department of Alcoholism of Erie County Medical Center, and the Clinical Research Center of the Research Institute on Addictions for allowing clients to participate in our study. Dr John Welte is acknowledged for consultation regarding statistical analyses.

Received February 27, 1996; first decision March 15, 1996; accepted March 15, 1996.


*    References
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowMethods
up arrowResults
up arrowDiscussion
*References
 
1. Neaton JD, Kuller L, Stamler J, Wentworth DN. Impact of systolic and diastolic blood pressure on cardiovascular mortality. In: Laragh JH, Brenner BM, eds. Hypertension: Pathophysiology, Diagnosis and Management. New York, NY: Raven Press Publishers; 1995:127-145.

2. Maheswaran R, Potter JF, Beevers DG. The role of alcohol in hypertension. J Clin Hypertens A. 1986;2:172-178.

3. Bonner LL, Kanter DS, Manson JE. Primary prevention of stroke. N Engl J Med. 1995;333:1392-1400.[Free Full Text]

4. Grobbee DE. Alcohol and blood pressure. In: Veenstra J, Vander Heij DG, eds. Alcohol and Cardiovascular Disease. Wageningen, Netherlands: Center for Agricultural Publishing and Documentation (Pudoc); 1992:23-35.

5. Keil V, Swales JD, Grobbee DE. Alcohol intake and its relation to hypertension. In: Verschuren PM, ed. Health Issues Related to Alcohol Consumption. Washington, DC: International Life Sciences Institute Press; 1993:18-42.

6. Klatsky AL. Blood pressure and alcohol intake. In: Laragh JH, Brenner BM, eds. Hypertension: Pathophysiology, Diagnosis and Management. 2nd ed. New York, NY: Raven Press Publishers; 1995:2649-2667.

7. Sorel JE. Alcohol and blood pressure. Epidemiology. 1994;5:567-569.[Medline] [Order article via Infotrieve]

8. Hirsch JA, Bishop B, York JL. Recovery of respiratory sinus arrhythmia with abstinence in detoxified alcoholics. J Appl Physiol. 1993;74:1816-1823.[Abstract/Free Full Text]

9. York JL, Biederman I. Hand movement speed and accuracy in detoxified alcoholics. Alcohol Clin Exp Res. 1991;15:982-990.[Medline] [Order article via Infotrieve]

10. York JL, Hirsch, JA. Drinking patterns and health status in smoking and nonsmoking alcoholics. Alcohol Clin Exp Res. 1995;19:666-673.[Medline] [Order article via Infotrieve]

11. Verschuren PM, ed. Health Issues Related to Alcohol Consumption. Washington, DC: International Life Sciences Institute Press; 1993.

12. York JL, Welte JW. Gender comparisons of alcohol consumption in alcoholic and nonalcoholic populations. J Stud Alcohol. 1994;55:743-750.[Medline] [Order article via Infotrieve]

13. York JL. Progression of alcohol consumption across the drinking career in alcoholics and social drinkers. J Stud Alcohol. 1995;56:328-336.[Medline] [Order article via Infotrieve]

14. York JL, Pendergast DE. Body composition in detoxified alcoholics. Alcohol Clin Exp Res. 1991;15:982-990.

15. York JL, Hirsch JA. Application of bioelectric impedance methodology and prediction equations to determine the volume of distribution for ethanol. Alcohol. 1995;12:553-558.[Medline] [Order article via Infotrieve]

16. Baecke JA, Burema J, Frijers JE. A short questionnaire for the measurement of habitual physical activity in epidemiological studies. Am J Clin Nutr. 1982;36:936-942.[Abstract/Free Full Text]

17. Moos RH. Health and Daily Living Form Manual. Palo Alto, Calif: Social Ecology Laboratory, Veterans Administration and Stanford University Medical Center; 1984.

18. Hollingshead AB, Redlich FC. Social Class and Mental Illness. New York, NY: John Wiley & Sons; 1958.

19. Skinner HA, Horn JL. Alcohol Dependence Scale (ADS). Users Guide. Toronto, Canada: Addiction Research Foundation; 1984.

20. Skinner HA, Sheu WJ. Reliability of alcohol use indices: the lifetime drinking history and the MAST. J Stud Alcohol. 1982;43:1157-1170.[Medline] [Order article via Infotrieve]

21. Harger RN, Hulpieu HR. The pharmacology of alcohol. In: Thompson GN, ed. Alcoholism. Springfield, Ill: Charles C Thomas, Publisher; 1956:103-232.

22. Watson PE. Total body water and blood alcohol levels: updating the fundamentals. In: Crow KE, Batt RD, eds. Human Metabolism of Alcohol. Boca Raton, Fla: CRC Press, Inc; 1989;1:45-56.

23. Hall WD, Saunders E, Shulman N. Hypertension in Blacks: Epidemiology, Pathophysiology and Treatment. Chicago, Ill: Year Book Medical Publishers, Inc; 1985.

24. Grim CE, Henry JP, Myers H. High blood pressure in blacks: salt, slavery, survival, stress, and racism. In: Laragh JH, Brenner BM, eds. Hypertension: Pathophysiology, Diagnosis and Management. New York, NY: Raven Press Publishers; 1995:171-206.

25. Klatsky AL, Friedman GD, Armstrong MA. The relationships between alcohol beverage use and other traits to blood pressure: a new Kaiser-Permanente study. Circulation. 1986;73:628-636.[Abstract/Free Full Text]

26. York JL. Influence of self-titration on the relationship between ethanol dose and chronic tissue toxicities: theoretical considerations. Alcohol. 1994;11:219-223.[Medline] [Order article via Infotrieve]

27. Savdie E, Grosslight GM, Adena MA. Relationship of alcohol and cigarette consumption to blood pressure and serum creatinine levels. J Chron Dis. 1984;37:617-623.[Medline] [Order article via Infotrieve]

28. Clark LT, Friedman HS. Hypertension associated with alcohol withdrawal: assessment of mechanisms and complications. Alcohol Clin Exp Res. 1985;9:125-130.[Medline] [Order article via Infotrieve]

29. MacMahon S. Alcohol consumption and hypertension. Hypertension. 1987;9:111-121.[Abstract/Free Full Text]

30. Urbano-Marquez A, Estruch R, Navarro-Lopez F, Grau JM, Mont L, Rubin E. The effects of alcoholism on skeletal and cardiac muscle. N Engl J Med. 1989;320:409-415.[Abstract]

31. Urbano-Marquez A, Estruch R, Fernandez-Sola J, Nicholas JM, Pare JC, Rubin E. The greater risk of alcoholic cardiomyopathy and myopathy in women compared to men. JAMA. 1995;274:149-154.[Abstract/Free Full Text]

32. Potter JF, Beevers DG. Pressor effect of alcohol in hypertension. Lancet. 1984;1:119-122.[Medline] [Order article via Infotrieve]

33. Randin D, Vollenweider P, Tappy L, Jequier E, Nicod P, Scherrer U. Suppression of alcohol-induced hypertension by dexamethasone. N Engl J Med. 1995;332:1733-1737.[Abstract/Free Full Text]

34. Victor RG, Hansen J. Alcohol and blood pressure: a drink a day. N Engl J Med. 1995;332:1782-1783.[Free Full Text]

35. Puddey IB, Beilin LJ, Vandongen R, Rouse IL, Rogers P. Evidence for a direct effect of alcohol consumption on blood pressure in normotensive men: a randomized controlled trial. Hypertension. 1985;7:707-713.[Abstract/Free Full Text]

36. King AC, Parsons OA, Bernardy NC, Lovallo WR. Drinking history is related to persistent blood pressure dysregulation in postwithdrawal alcoholics. Alcohol Clin Exp Res. 1994;18:1172-1176.[Medline] [Order article via Infotrieve]




This article has been cited by other articles:


Home page
Alcohol AlcoholHome page
M. CECCANTI, G. F. SASSO, R. NOCENTE, G. BALDUCCI, A. PRASTARO, C. TICCHI, G. BERTAZZONI, P. SANTINI, and M. L. ATTILIA
HYPERTENSION IN EARLY ALCOHOL WITHDRAWAL IN CHRONIC ALCOHOLICS
Alcohol Alcohol., January 1, 2006; 41(1): 5 - 10.
[Abstract] [Full Text] [PDF]


Home page
HypertensionHome page
C. Di Gennaro, A. Barilli, C. Giuffredi, C. Gatti, A. Montanari, and P. P. Vescovi
Sodium Sensitivity of Blood Pressure in Long-Term Detoxified Alcoholics
Hypertension, April 1, 2000; 35(4): 869 - 874.
[Abstract] [Full Text] [PDF]


Home page
HypertensionHome page
K. Seppa and P. Sillanaukee
Binge Drinking and Ambulatory Blood Pressure
Hypertension, January 1, 1999; 33(1): 79 - 82.
[Abstract] [Full Text] [PDF]


This Article
Right arrow Abstract Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by York, J. L.
Right arrow Articles by Hirsch, J. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by York, J. L.
Right arrow Articles by Hirsch, J. A.