Pressor Effect of Moderate Alcohol Consumption in Man: A Proposed Mechanism

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

doi:10.1111/j.1440-1681.1983.tb00216.x

Cited by 9 publications

(5 citation statements)

References 11 publications

(5 reference statements)

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“…In contrast to findings of the effect of one-time moderate alcohol consumption (0.5-0.75 g of ethanol/kg or 2 drinks) on sympathetic activity in young adults [17][18][19][20][21], we found that MODs did not have increased urinary NE levels compared with ABs. It has been suggested that alcohol-induced sympathetic activity may be dose dependent, with no effect of alcohol consumption at low level (1 drink) [21].…”

Section: Discussioncontrasting

confidence: 99%

“…Several studies have examined the effect of alcohol consumption on sympathetic activation and there are data supporting the scientific premise that alcohol consumption in young adults may be associated with increased sympathetic activation. However, studies to date have only examined the effect of a "single, one-time" binge or moderate drinking episode [15][16][17][18][19][20][21].…”

Section: Introductionmentioning

confidence: 99%

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The effects of repeated binge drinking on arterial stiffness and urinary norepinephrine levels in young adults

Hwang

Piano

Hill

et al. 2020

Journal of Hypertension

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Objectives: To investigate the effect of repeated binge drinking and moderate alcohol consumption in young adults on arterial stiffness and sympathetic activity in young adults Methods: We enrolled 49 healthy young adults, free of cardiovascular diseases (25 males; age: 23.5±0.4 years; body mass index: 23.4±0.4 kg/m2; mean±S.E). Subjects included were those with a history of repeated binge drinking (BDs, > 2 years duration; n=20), drank at moderate levels (MODs, > 5 years duration; n=16), and abstained from alcohol (ABs, last 2-3 years; n=13). Arterial stiffness was assessed using carotid to femoral pulse wave velocity (cfPWV) and sympathetic activity was assessed using 24-hour urinary norepinephrine (NE) levels. Also measured was aortic systolic blood pressure and augmentation index (AIx), a measure of wave reflection.Results: BDs and MODs had higher cfPWV compared with ABs (0.6 and 0.5 m/sec, respectively; P≤0.04). In addition, BDs had higher urinary NE levels compared with MODs and ABs (P<0.05). Higher cfPWV were correlated with higher NE levels (r=0.35. P=0.02). Aortic systolic blood pressure (P=0.2) and AIx (P=0.96) were similar among BDs, MODs, and ABs. Conclusions:Our findings suggest that repeated exposure to alcohol, regardless of drinking pattern, may increase aortic arterial stiffness in healthy young adults. In addition, sympathetic activation, reflected by increased 24-hour urinary NE levels may contribute to alcohol-induced arterial stiffening in young adults.

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Section: Discussioncontrasting

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The effects of repeated binge drinking on arterial stiffness and urinary norepinephrine levels in young adults

Hwang

Piano

Hill

et al. 2020

Journal of Hypertension

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“…There is now good evidence for a direct pressor effect of regular alcohol consumption in man (Puddey et al 1985a). Our attempts to understand the mechanism of such an effect have so far addressed possible influences o n sympatho-adrenergic mechanisms (Ireland et al 1983), the renin-angiotensin axis (Puddey et al 1985b), membrane sodium handling (Puddey et al 1986) and calcium metabolism (Arkwright et al 1984).…”

Section: Discussionmentioning

confidence: 99%

Urinary Steroid Profiles and Alochol‐related Blood Pressure Elevation

Mori

Puddey

Wilkinson

et al. 1991

Clin Exp Pharma Physio

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1. From an earlier cross-sectional survey of 343 public servants, 15 pairs of non-smoking teetotallers and heavy drinkers (alcohol intake more than 350 mL/week) were matched for age and adiposity and utilized for a case-control study of the effects of alcohol on 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD) activity and blood pressure. 2. Two successive 24 h urine collections were analysed by radio-immunoassay (RIA) for cortisol excretion, and for the cortisol and cortisone metabolites, tetrahydrocortisol (THC), allo-tetrahydrocortisol (allo-THC) and tetrahydrocortisone (THE), by capillary column gas chromatography. 3. Heavy drinkers had higher systolic and diastolic blood pressure (BP) than teetotallers (132.6 +/- 2.5 vs 123.2 +/- 1.3 and 78.7 +/- 1.6 vs 71.7 +/- 1.4, respectively; unpaired t-test, P less than 0.01). Twenty-four-hour urinary sodium and cortisol excretion were similar in the two groups. 4. The THC plus allo-THC:THE ratio was similar in drinkers and teetotallers (1.81 +/- 0.20 vs 2.03 +/- 0.20), consistent with no effect of alcohol on 11 beta-OHSD activity. The ratio of THC to allo-THC was increased in drinkers compared with teetotallers (1.49 +/- 0.18 vs 1.05 +/- 0.13; unpaired t-test, P less than 0.05), consistent with either a decrease in 5 alpha-reductase activity or an increase in 5 beta-reductase activity. 5. This study provides no evidence for alcohol-related inhibition of 11 beta-OHSD, despite substantially higher blood pressures in heavy drinkers compared to teetotallers. Such an effect is, therefore, unlikely to contribute significantly to the mechanism of alcohol-related hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…Older studies showed roles for the sympathetic and central nervous systems in the elevation of blood pressure that occurs in the hours following ethanol ingestion [25], as well as in cellular divalent ion dysregulation [26]. Other proposed mechanisms are detailed in Table 1.…”

Section: Mechanismsmentioning

confidence: 98%

Alcohol and its relationship to blood pressure

Kodavali¹,

Townsend

2006

Current Science Inc

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Ethanol is a molecule of enduring research interest because its consumption has important social as well as medical implications. With excessive ethanol consumption, there is higher prevalence for hypertension, stroke, cardiomyopathy, and arrhythmias. A principal mechanism by which ethanol exerts these cardiovascular effects is through modulation of blood pressure. In this article, we focus on recent research that pursues information on the effects of alcohol on blood pressure in human subjects, regardless of whether they have hypertension or not. Known means by which alcohol exerts hemodynamic effects are briefly covered, and insights on novel biomediators, such as endothelin and gene-based mechanisms, are presented. Newer tools, such as the Alcohol Use Disorders Identification Test-Consumption Questions (AUDIT-C) survey and carbohydrate-deficient transferrin (CDT) serum test, are also covered. Reducing excessive alcohol intake can produce a reduction in blood pressure of up to 4 mm Hg, on average, which could substantially affect the rates of stroke and ischemic heart disease.

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Pressor Effect of Moderate Alcohol Consumption in Man: A Proposed Mechanism

Cited by 9 publications

References 11 publications

The effects of repeated binge drinking on arterial stiffness and urinary norepinephrine levels in young adults

The effects of repeated binge drinking on arterial stiffness and urinary norepinephrine levels in young adults

Urinary Steroid Profiles and Alochol‐related Blood Pressure Elevation

Alcohol and its relationship to blood pressure

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