Acute effects of moderate alcohol consumption on blood pressure and plasma catecholamines

Ireland, Mark A.; Vandongen, R.; Davidson, Lisa; Beilin, Lawrence J.; Rouse, Ian

doi:10.1042/cs0660643

Cited by 169 publications

(84 citation statements)

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“…Child et al 31 suggested the positive chronotropic effect of ethanol is mediated by sympathetic overactivity that was sufficient to mask its cardiodepressant effect. Other investigators 20 have provided a more direct evidence that showed that ethanol caused a relative increase in plasma epinephrine levels during the ascending phase of the blood ethanol curve in normotensive human volunteers. The most direct evidence that shows ethanol increases central sympathetic tone came from our laboratory.…”

Section: Discussionmentioning

confidence: 99%

“…We decided, however, to use a dose of ethanol that resulted in a blood ethanol concentration of 54.2±6.3 mg/dl, which is comparable to that attained after social drinking. 20 This dose of ethanol, 1 g/kg, produced an upward shift of the clonidine dosedepressor response curve and resulted in a significant attenuation of the depressor response to the same dose of clonidine (Figure 3). Based on this finding, if the dose of clonidine is adjusted to produce the desired decrease in pressure of an alcohol user, care should be taken not to advise abrupt abstinence of alcohol consumption, otherwise an exaggerated depressor response to clonidine may ensue.…”

Section: -14mentioning

confidence: 99%

“…12 -14 On the other hand, even though alcohol does not change blood pressure after its acute administration, 15 -17 it increases heart rate, 16 -18 sympathetic efferent discharge, 19 and circulating levels of catecholamines. 20 Also, both alcohol and clonidine influence differently the baroreceptor reflexes. Whereas clonidine sensitizes the baroreceptor heart rate response, 21 -22 and this effect may contribute to its antihypertensive effect, 23 alcohol impairs this reflex response.…”

Section: Reversal By Ethanol Of the Hypotensive Effect Of Clonidine Imentioning

confidence: 99%

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Reversal by ethanol of the hypotensive effect of clonidine in conscious spontaneously hypertensive rats.

Abdel‐Rahman

1989

Hypertension

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We studied the acute effect of ethanol on the hypotensive response to clonidine in conscious spontaneously hypertensive rats. When administered during the hypotensive response to clonidine, ethanol not only reversed the response but also caused a slight but significant short-lived pressor effect. The maximal hypotensive effect of graded doses of clonidine was significantly (p<0.05) attenuated by a dose of 1 g/kg ethanol, which resulted in a peak blood ethanol concentration of 54.2 ±6.3 mg/dl. The data strongly suggest the adverse effect of ethanol on the hypotensive response to clonidine is ethanol mediated and that their antagonistic interaction is both reversible and reproducible because: 1) an equal volume of saline had no effect on the hemodynamic responses to clonidine and 2) crossing over ethanol and saline treatments on days 2 and 3, which allowed longitudinal comparisons, showed that the effect of ethanol was similar both in naive rats (day 1) and in rats that were pre-exposed to ethanol (day 3). Whether this negative effect of ethanol also involves other antihypertensive agents that do not act primarily by a central nervous system mechanism was investigated. The same dose of ethanol had little or no effect on the hypotensive response to hydralazine, suggesting the negative effect of ethanol is selective to centrally acting antihypertensive agents. Although the mechanism by which ethanol reverses the hypotensive effect of clonidine is not known, it is possible that it involves an ethanol-evoked increase in plasma catecholamine levels, which are known to be decreased by clonidine. That ethanol did not reverse the hypotensive effect of hydralazine, which is also known to be associated with increased plasma catecholamine levels, supports this notion. The findings of the present study may explain, at least in part, why regular use of alcohol is associated with an inadequate control of blood pressure in treated hypertensive patients who are regular consumers of alcohol. (Hypertension 1989;14:531-541)

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Section: Discussionmentioning

confidence: 99%

Section: -14mentioning

confidence: 99%

Section: Reversal By Ethanol Of the Hypotensive Effect Of Clonidine Imentioning

confidence: 99%

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Reversal by ethanol of the hypotensive effect of clonidine in conscious spontaneously hypertensive rats.

Abdel‐Rahman

1989

Hypertension

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“…Some studies have shown an increase in BP, 13,14 whereas it decreased 15,16 or remained unchanged 17,18 in others. In hypertensive patients, the BP also became elevated 19 or fell 20 after a single ingestion of alcohol.…”

Section: Cardiovascular 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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“…It has been proposed that alcohol consumption relieves anxiety and thus may help the individual to cope with stress (Hodgson et al 1979;Vogel and De Turck 1983;Pohorecky 1991). However, a number of studies indicate that alcohol can either reduce or produce anxiety (Cappell and Herman 1972;Hodgson et al 1979;Malford 1983;Cappell and Greely 1987;Pohorecky 1991), depending on the experimental conditions used, such as the dose of alcohol (Klatsky et al 1977;De Turck and Vogel 1982;Kelbaek et al 1985), prior exposure to alcohol (Ireland et al 1984;Marmot 1984) and whether or not the subject was stressed at the time of the study (Pohorecky 1981(Pohorecky , 1991. In designing studies investigating how ethanol influences stress responses, it is reasonable to investigate biological systems affected by both ethanol and stress.…”

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confidence: 99%

Response of the Hypothalamic-Pituitary-Adrenal Axis to Stress in the Absence and Presence of Ethanol in Subjects at High and Low Risk of Alcoholism,

Dai

2002

Neuropsychopharmacology

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Both genetic and environmental factors, such as stress, are important in determining alcohol consumption. Furthermore, both stress and alcohol influence the activity of the hypothalamic-pituitary-adrenal (HPA)-axis. Thus, the present studies investigated the response of the HPA axis to stress and the effect of ethanol on the stress response, in subjects at high (HR) and low (LR) risk of alcoholism as determined from their family history. Twenty HR and 20 LR subjects performed a stress-inducing task 30 min following the ingestion of either a placebo drink or a low dose of ethanol. The levels of plasma adrenal corticotropic hormone (ACTH) and cortisol were measured prior to and for four hours following initiation of the treatment. Changes with time in the plasma hormone levels following ingestion of either a placebo or an ethanol drink, without the performance of the stress task, served as controls to compare the stress-induced changes. Neither the placebo nor the ethanol drink altered the plasma ACTH and cortisol concentrations. High risk subjects presented lower basal ACTH, but not cortisol, levels and a lower stress-induced increase in plasma ACTH concentration than LR subjects. Furthermore, the HR subjects presented a delayed poststress recovery of the plasma ACTH and cortisol levels. Ethanol consumption prior to the stress task attenuated (ACTH) or abolished (cortisol) the stress-induced increaseExperimental evidence indicates that both genetic and environmental factors play a significant role in determining alcohol consumption (Light et al. 1996). Studies using human subjects and experimental animals have demonstrated that stress is one of the environmental factors associated with the initiation and continuation of heavy drinking, as well as relapse (Hore 1971;Kushner et al. 1990;Pohorecky 1991;De Wit 1996;Le et al. 1998;Stewart 2000). Indeed, it has been shown that alcohol consumption increases in response to stress if The studies in the present manuscript were presented at the Annual Meeting of the Society for Neuroscience, on November 6, 2000, at New Orleans LA. Abstracts Society for Neuroscience 2000: Vol. 26, Abstract # 300.10, p.803.Address correspondence to: Christina Gianoulakis, Ph.D., Douglas Hospital Research Centre, 6875 LaSalle Blvd, Verdun, Quebec, Canada H4H 1R3. Tel.: (514) ext 5929; Fax:(514) 762-3034; E-mail: christina.gianoulakis@mcgill.ca Received July 24, 2001; revised November 26, 2001; accepted February 8, 2002. Online publication: 2/14/02 at www.acnp.org/citations/Npp 021402245.N EUROPSYCHOPHARMACOLOGY 2002 -VOL . 27 , NO . 3 Ethanol, Stress, the HPA Axis, and Family History of Alcoholism 443 other forms of support, such as social and family support, are not present (Pohorecky 1991;Johnson and Jennison 1994). The mechanisms underlying the relationship between stress and alcohol consumption are not well understood. It has been proposed that alcohol consumption relieves anxiety and thus may help the individual to cope with stress (Hodgson et al. 1979;Vogel and De Turck 198...

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Acute effects of moderate alcohol consumption on blood pressure and plasma catecholamines

Cited by 169 publications

References 16 publications

Reversal by ethanol of the hypotensive effect of clonidine in conscious spontaneously hypertensive rats.

Reversal by ethanol of the hypotensive effect of clonidine in conscious spontaneously hypertensive rats.

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

Response of the Hypothalamic-Pituitary-Adrenal Axis to Stress in the Absence and Presence of Ethanol in Subjects at High and Low Risk of Alcoholism,

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