Suppression of Alcohol-Induced Hypertension by Dexamethasone

Randin, D; Vollenweider, Péter; Tappy, Luc; Jéquier, E; Nicod, Pascal; Scherrer, Urs

doi:10.1056/nejm199506293322601

Cited by 162 publications

(108 citation statements)

References 25 publications

(46 reference statements)

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“…26 It has been reported that dexamethasone inhibited the BP elevation and sympathetic activation after alcohol ingestion. 45 We and others, however, have failed to observe significant changes in adrenocorticotropic hormone, cortisol or aldosterone. 21,42 Alcohol suppresses the release of vasopressin; however, this change does not seem to mediate the acute depressor effect of alcohol.…”

Section: Neurohormonal Actions Of Alcoholmentioning

confidence: 99%

Physio-pathological effects of alcohol on the cardiovascular system: its role in hypertension and cardiovascular disease

Kawano

2010

Hypertens Res

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Alcohol has complex effects on the cardiovascular system. The purpose of this article is to review physio-pathological effects of alcohol on cardiovascular and related systems and to describe its role in hypertension and cardiovascular disease. The relationship between alcohol and hypertension is well known, and a reduction in the alcohol intake is widely recommended in the management of hypertension. Moreover, alcohol has both pressor and depressor actions. The latter actions are clear in Oriental subjects, especially in those who show alcohol flush because of the genetic variation in aldehyde dehydrogenase activity. Repeated alcohol intake in the evening causes an elevation in daytime and a reduction in nighttime blood pressure (BP), with little change in the average 24-h BP in Japanese men. Thus, the hypertensive effect of alcohol seems to be overestimated by the measurement of casual BP during the day. Heavy alcohol intake seems to increase the risk of several cardiovascular diseases, such as hemorrhagic stroke, arrhythmia and heart failure. On the other hand, alcohol may act to prevent atherosclerosis and to decrease the risk of ischemic heart disease, mainly by increasing HDL cholesterol and inhibiting thrombus formation. A J-or U-shaped relationship has been observed between the level of alcohol intake and risk of cardiovascular mortality and total mortality. It is reasonable to reduce the alcohol intake to less than 30 ml per day for men and 15 ml per day for women in the management of hypertension. As a small amount of alcohol seems to be beneficial, abstinence from alcohol is not recommended to prevent cardiovascular disease. INTRODUCTIONAlcohol has complex effects on the cardiovascular system. The relationship between alcohol and hypertension is well known, and a restriction of alcohol intake is widely recommended as a part of lifestyle modifications in the management of hypertension. 1-6 Alcohol has both pressor and depressor actions, however, and the genetic susceptibility regarding alcohol metabolism influences the cardiovascular effect of alcohol. 3,7 The effect of alcohol on blood pressure (BP) is also modified by several factors, such as the level of consumption, time period after the last drink and overall drinking behavior.Alcohol consumption is associated with several cardiovascular diseases, such as brain hemorrhage, heart failure and arrhythmia, as well as with other disorders. 3,[8][9][10][11] Heavy drinking and alcoholism not only lead to medical problems but are also serious social concerns. However, alcohol also seems to have beneficial effects, including the prevention of ischemic heart disease. It has been shown that cardiovascular and all-cause mortality is lower in light drinkers compared with nondrinkers. 3,[8][9][10][11][12] The purpose of this article is to review physio-pathological effects of alcohol on cardiovascular and related systems and to describe its role

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Section: Neurohormonal Actions Of Alcoholmentioning

confidence: 99%

Physio-pathological effects of alcohol on the cardiovascular system: its role in hypertension and cardiovascular disease

Kawano

2010

Hypertens Res

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“…4 Human studies have found that acute alcohol intake induces elevations of heart rate and blood pressure via centrally mediated increases of sympathetic discharge. 5 There is also evidence that abnormalities of cardiovascular regulation persist into recovery. Abstinent alcohol-dependent male patients show exaggerated heart rate and blood pressure reactivity in response to behavioral stress, although measures of sympathetic activation have not been determined.…”

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confidence: 99%

Sleep Deprivation Potentiates Activation of Cardiovascular and Catecholamine Responses in Abstinent Alcoholics

Irwin

2005

Hypertension

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Abstract-Alcohol dependence is associated with an increased incidence of hypertension and cardiac arrhythmias, but the triggering mechanisms are not known. Sleep loss, common in alcohol-dependent patients, causes an activation of the sympathetic nervous system. To determine whether sleep deprivation induces differential cardiovascular and sympathetic responses in alcohol dependence, we measured heart rate, blood pressure, and circulating sympathetic catecholamines in 36 abstinent alcohol-dependent men and 36 age-, gender-, and ethnicity-matched controls after a baseline night of sleep, in the morning after early night partial sleep deprivation, and again after a full night of recovery sleep. Subjects were on average normotensive and none was being treated for hypertension. Baseline heart rate, blood pressure, and sympathetic catecholamines were similar in the 2 groups. Administration of partial night sleep deprivation induced greater increases of heart rate (PϽ0.01) and circulating levels of norepinephrine (PϽ0.05) and epinephrine (PϽ0.05) in the alcohol-dependent men as compared with responses in controls. Even after a full night of recovery sleep, elevations in heart rate (PϽ0.05) and circulating catecholamines (PϽ0.05) persisted in the alcoholic subjects. Partial night sleep deprivation induces elevated heart rate and sympathetic catecholamine responses in alcoholic subjects as compared with controls, and this sympathetic activation is sustained after nights of partial and recovery sleep. A lcohol dependence, which exceeds a lifetime incidence of 10%, 1 is a major risk factor for cardiovascular diseases, with alcohol-dependent men showing an increased prevalence of hypertension and cardiac arrhythmias. 2,3 An increase of sympathetic nervous system activity is implicated as being one underlying mechanism of the deleterious cardiovascular effects of chronic alcohol consumption. 4 Human studies have found that acute alcohol intake induces elevations of heart rate and blood pressure via centrally mediated increases of sympathetic discharge. 5 There is also evidence that abnormalities of cardiovascular regulation persist into recovery. Abstinent alcohol-dependent male patients show exaggerated heart rate and blood pressure reactivity in response to behavioral stress, although measures of sympathetic activation have not been determined. 6 -8 In this study, we examined cardiovascular responses and circulating levels of norepinephrine and epinephrine at rest and in response to a behavioral challenge, sleep deprivation, in abstinent male alcohol-dependent patients.Experimental sleep deprivation can serve as a naturalistic probe of the homeostatic regulation of sympathetic activity. Loss of sleep induces elevations in circulating levels of epinephrine and norepinephrine, 9,10 with attendant increases of blood pressure and heart rate the next day. 11,12 In addition, habitual sleep loss and insomnia are markers of subclinical heart disease and are independent predictors of cardiovascular disease risk, particularly in ma...

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“…Infusions of acetate, however, do not reduce insulin-mediated glucose utilization, indicating that ethanol-induced insulin resistance does not result from substrate competition in the strict sense of the term (38). A possible explanation for ethanol-induced insulin resistance is activation of muscle sympathetic nerve activity which occurs following acute ethanol administration (39). Indeed, it has been observed that stimulation of sympathetic activity attained by application of lower body negative pressure decreases insulin sensitivity by mechanisms which remain to be determined (40,41).…”

Section: Figurementioning

confidence: 99%