Renin, aldosterone and Cortisol during ethanol intoxication and hangover

Linkola, Jaakko; Fyhrquist, Frej; Ylikahri, Reino

doi:10.1111/j.1748-1716.1979.tb06372.x

Cited by 80 publications

(31 citation statements)

References 30 publications

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“…Urinary excretion of epinephrine is greater during withdrawal than during alcohol administration," and plasma norepinephrine levels are highest 13 to 24 hours after alcohol cessation." In addition, plasma arginine vasopressin" and plasma renin activity 37 are increased during the withdrawal phase. Whether the effect on BP begins during the alcohol intoxication or withdrawal period is of more physiologic than clinical interest, since either way the effect is due to alcohol.…”

Section: Discussionmentioning

confidence: 99%

Alcohol consumption and blood pressure. The lipid research clinics prevalence study.

Criqui¹,

Wallace²,

Mishkel³

et al. 1981

Hypertension

177

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The relationship between alcohol consumption and systolic and diastolic blood pressure (BP) was examined in 2482 men and 2301 women 20 years of age or older in nine North American populations. Men at the highest level of alcohol consumption (^ 30 ml alcohol per day) had the highest BP, while women either at the highest lerel of alcohol consumption or consuming no alcohol had the highest BP. Men aged 5: 35 years of age consuming S 30 ml alcohol per day were 1.5 to 2 times more likely to be hypertensive than non-drinkers. Multivariate analysis showed systolic and diastolic BP in both men and women to be positively and significantly (p < 0.05) related to alcohol consumption, and this relationship was independent of the potential confounding effects of age, obesity, cigarette smoking, regular exercise, education, and gonadal hormone use in women. The regression coefficients indicated that an average of 30 ml of alcohol per day would produce a 2 to 6 mm Hg increase in systolic BP. Analyses suggested the univariate U-shaped alcohol-BP association in women was confounded by differences in obesity and cigarette smoking in nondrinking women, and by very low alcohol consumption in hypertensive women using medication. Additional analyses indicated that alcohol consumed in the 24 hours prior to the study was much more strongly associated with elevated BP than alcohol consumed in the week prior to the study excluding the previous 24 hours. We conclude that alcohol appears to have a modest but consistent and independent effect on systolic and diastolic BP. (Hypertension 3: 557-565, 1981) KEY WORDS • hypertension cigarette smoking eplderaiologlc studies • population studies • obesity T HERE is mounting evidence from both clinical and epidemiologic studies that alcohol consumption , especially at higher levels, is associated with elevations in blood pressure (BP), both systolic and diastolic, although the elevation in systolic BP is generally of greater magnitude. Previous studies have varied greatly in their assessment of both alcohol consumption and BP, and in their assessment of potential confounding factors that might be involved in this association. A consistent finding has been that drinkers at the highest levels of alcohol consumption show an increase in BP. 110 Other studies have shown an increase in liver function abnormalities in hypertensive patients, presumably due to increased alcohol intake. 11 ' u However, some studies have indicated certain subsets of drinkers of small or moderate amounts of alcohol had BPs no higher or even lower than non-drinkers. 1 " 8 In addition, most acute challenge studies in both animals and human subjects have shown little or no short-term effect of alcohol on BP, 1 '" 20 although positive results have been reported. 12 ' M Studies of chronic alcohol administration in animals have reported no significant long-term effect on BP. MM If alcohol can indeed raise BP, how can the nonlinear relationship in some epidemiologic studies and the uncertain results from challenge studies be explained...

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Section: Discussionmentioning

confidence: 99%

Alcohol consumption and blood pressure. The lipid research clinics prevalence study.

Criqui¹,

Wallace²,

Mishkel³

et al. 1981

Hypertension

177

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“…Gill et al 33 noted similar changes in urea and suggested that the alcohol-induced diuresis may have led to increased urea clearance. Linkola et al 34 noted an initial suppression of plasma renin activity following alcohol ingestion and found that plasma renin activity rose only during the hangover period. Changes in the renin-angiotensin-aldosterone axis do not appear to account for the rise in blood pressure with alcohol ingestion.…”

Section: Figure 3 Effect Of Alcohol (*) and Placebo (O) On Plasma Nomentioning

confidence: 99%

“…A similar fall has been noted by other workers, and levels usually do not rise until the withdrawal period. 34 The acute, alcohol-induced elevations of plasma cortisol have been reported to be related to the degree of discomfort and usually are not encountered with blood alcohol levels below 100 mg/dl.…”

Section: Figure 3 Effect Of Alcohol (*) and Placebo (O) On Plasma Nomentioning

confidence: 99%

The pressor and metabolic effects of alcohol in normotensive subjects.

Potter¹,

Watson²,

Skan³

et al. 1986

Hypertension

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SUMMARY Changes in blood pressure, pulse rate, and plasma catecholamines, renin activity, cortisol, and calcium were studied in 16 normotensive subjects (eight with a family history of hypertension) for 5 hours following ingestion of alcohol-free and alcohol-loaded beer. Both systolic and diastolic blood pressure rose after alcohol consumption; maximum responses occurred at peak blood alcohol concentrations and were significantly higher than those seen after placebo. Pulse rate was also significantly higher after alcohol ingestion and continued to rise throughout the study. There was no difference in the pressor response to alcohol between the groups with and without a family history of hypertension. No difference was found in plasma norepinephrine or epinephrine levels between alcohol and placebo phases. However, subjects with no family history of hypertension had significantly higher plasma norepinephrine levels (p<0.01) than did those with a family history during both the alcohol and placebo phases, although baseline blood pressures were not significantly different. Plasma epinephrine level was similar in both groups. Plasma renin activity was unchanged throughout, but plasma cortisol fell during both phases. Plasma calcium showed a small but significant fall with alcohol consumption in both groups (p<0.001). These results indicate that in normotensive subjects alcohol ingestion causes a rise in systolic and diastolic blood pressure that is not influenced by a family history of hypertension. This effect does not appear to be sympathetically mediated but may be due to a direct vasoconstrictor effect of alcohol, possibly with an alcohol-induced shift in intracellular calcium. Dr. Potter was supported by a research grant from the British Heart Foundation.Address for reprints: Dr. J.F. Potter, Freeman Road Hospital, Newcastle upon Tyne NE7 7DN, UK.Received July 19, 1985; accepted December 30, 1985. and the duration of the study. We have therefore examined, in normotensive subjects, the acute effects of alcohol and placebo on blood pressure in relation to the possible pressor mechanisms. We examined the changes in blood pressure with the rise and fall in blood alcohol levels to determine whether these changes were due to a direct effect of alcohol or were related to a withdrawal response. Subjects and Methods

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“…Several socio-economic factors for each prefecture were used in a stepwise multiple regression analysis. These factors were, the annual income per capita, the number of men per 100,000 who are receiving public aid, the number of tatamis (a Japanese traditional floor unit) per household, the unemployment rate per 100,000 men, the unmarried rate per 100 men aged [35][36][37][38][39][40][41][42][43][44][45][46][47][48][49] Age-adjusted stroke mortalities for all ages and for the middle-aged by sex, and the male:female ratio of age-adjusted stroke mortality for the middle-aged and all ages were used as dependent variables, while alcohol consumption, salt intake and socio-economic factors were used as independent variables in a stepwise multiple regression analysis. The same independent variables were used for the stepwise multiple regres- Table 1 shows the mean and standard deviations of the variables used in this study.…”

Section: Statistics For 46 Prefectures Excluding Okinawa Inmentioning

confidence: 99%

Regional differences in stroke mortality and alcohol consumption in Japan.

Ueshima¹,

Ohsaka²,

Asakura³

1986

Stroke

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SUMMARYThe relationship between alcohol consumption and stroke mortality in 1975 in 46 prefectures of Japan was investigated. This was done by adjusting salt intake and several socio-economic factors, i.e., the annual per capita income, the number of persons who received public aid, the number of tatamis (a Japanese traditional floor unit) per household, the unemployment rate, and the unmarried or divorce rate, using a stepwise multiple regression analysis. As dependent variables, the sex-specific and age-adjusted mortality for the middle-aged (35-59 years) and for all ages due to stroke were used. For men, alcohol consumption was significantly related to age-adjusted stroke mortalities for the middle-aged and for all ages independent of salt intake and several socio-economic factors. Alcohol consumption was more strongly related to age-adjusted stroke mortality for the middle-aged than for all ages. For women alcohol was weakly correlated with the stroke mortality of the middle-aged. Salt intake was significantly correlated with stroke mortality for women but not for men. Furthermore, the male: female ratios of the age-adjusted stroke mortality for the middle aged and for all ages were analyzed as well, because alcohol is mostly consumed by men in Japan, and it was expected that the sex ratios would be well correlated to alcohol consumption. The results were as expected. Therefore, it was suggested that the regional difference in stroke mortality in Japan may be explained in part by that of alcohol consumption. Stroke Vol 17, No 1, 1986STROKE has been one of the leading causes of death in Japan. 1 Hypertension is a major risk factor for stroke.2 ' 8 Mortality, the incidence of stroke, and the prevalence of hypertension have been higher in the northeastern than in the southwestern part of Japan. These areas with high stroke mortality and high prevalence of hypertension correspond to high salt intake.2 -9 "" However, alcohol intake is higher in the northeastern part of the main island (Honshu) of Japan, especially in Akita Prefecture, than in any other area. ' 2 It is well documented not only by cross-sectional epidemiological studies but also by follow-up studies that moderate or heavy level of alcohol drinking is related to hypertension.13 " 16 Furthermore, several animal and epidemiological studies suggest that alcohol is a risk factor for stroke independent of hypertension.6 -8 l7~22Therefore, whether or not the regional difference in stroke mortality across 46 prefectures is related to alcohol consumption, and independent of salt and several socio-economic factors in Japan, was analyzed by a stepwise multiple regression analysis. , excluding Okinawa, in 1975 were used to analyze the relationship between stroke mortality and alcohol consumption. Age-specific stroke mortality data by prefecture and sex were available in the Special Report of Vital Statistics in Japan, 1975. Materials and MethodsStatistics for 46 prefecturesM The age-adjusted stroke mortalities for all ages by sex were calculated using the na...

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Renin, aldosterone and Cortisol during ethanol intoxication and hangover

Cited by 80 publications

References 30 publications

Alcohol consumption and blood pressure. The lipid research clinics prevalence study.

Alcohol consumption and blood pressure. The lipid research clinics prevalence study.

The pressor and metabolic effects of alcohol in normotensive subjects.

Regional differences in stroke mortality and alcohol consumption in Japan.

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