Interaction of acetaldehyde with plasma proteins of the renin-angiotensin system

Thevananther, Sundararajah; Brecher, Arthur S.

doi:10.1016/0741-8329(94)90074-4

Cited by 30 publications

(21 citation statements)

References 33 publications

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“…In chronic alcohol drinkers, the elevation of acetaldehyde levels results in an increase in angiotensin I levels, an effect that might enhance the activity of the renin-angiotensin system cascade and, consequently, contribute to HT [35,36]. Acetaldehyde-mediated inhibition of angiotensin-converting enzyme activity could be responsible for transient acute vasodilation and facial flushing in response to alcohol [37].…”

Section: Discussionmentioning

confidence: 99%

Associations between aldehyde dehydrogenase 2 (ALDH2) genetic polymorphisms, drinking status, and hypertension risk in Japanese adult male workers: a case–control study

Ota

Hisada

et al. 2015

Environ Health Prev Med

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Objectives We sought to identify associations between aldehyde dehydrogenase 2 (ALDH2), alcohol consumption, and hypertension in Japanese men. Methods The study participants were 1,225 male Japanese workers. We collected lifestyle information, body measurements, blood biochemical parameters, blood pressure measurements, and ALDH2 genotyping data during medical examinations conducted between March 2004 and January 2005 at a work facility and an affiliated company. Lifestyle data on alcohol intake and smoking were collected using self-administered questionnaires at the same time as when the aforementioned measurements were obtained. Results The genotype frequencies of ALDH2 genetic polymorphisms were 62.6, 32.7, and 4.7 % for

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Section: Discussionmentioning

confidence: 99%

Associations between aldehyde dehydrogenase 2 (ALDH2) genetic polymorphisms, drinking status, and hypertension risk in Japanese adult male workers: a case–control study

Ota

Hisada

et al. 2015

Environ Health Prev Med

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“…37 Alcohol could also lower fibrinolytic potential through activation of the reninangiotensin system, 38 either by volume depletion caused by inhibition of vasopressin release 39 or a direct effect of acetaldehyde. 40 Finally, heavy alcohol consumption affects coagulation by damaging the synthetic capacity of hepatocytes, both directly and through metabolites, but it is uncertain whether moderate alcohol intake acts similarly. 36 …”

Section: Discussionmentioning

confidence: 99%

Alcohol Consumption and Hemostatic Factors

et al. 2001

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Background-Moderate alcohol consumers have lower rates of cardiovascular disease than abstainers. One proposed mechanism is a beneficial effect on hemostatic parameters, but previous studies have provided conflicting results. Methods and Results-We measured levels of fibrinogen, plasma viscosity, von Willebrand factor, factor VII, plasminogen activator inhibitor antigen-1, and tissue plasminogen activator antigen in a cross-sectional analysis of 3223 adults free of cardiovascular disease enrolled in the Framingham Offspring Study. We assessed their alcohol consumption with a standardized questionnaire. Light-to-moderate alcohol consumption was associated with lower levels of fibrinogen, plasma viscosity, von Willebrand factor, and factor VII. This association was most pronounced for consumers of 3 to 7 drinks weekly for viscosity and 7 to 21 drinks weekly for the other hemostatic measures. Alcohol intake of 7 to 21 drinks weekly or more was associated with impaired fibrinolytic potential, reflected by higher levels of plasminogen activator inhibitor antigen-1 and tissue plasminogen activator antigen. Wine drinkers had lower plasminogen activator inhibitor antigen-1 levels than other drinkers, particularly at 3 to 21 drinks weekly, but beverage type did not otherwise consistently affect the results. Conclusions-Light-to-moderate alcohol consumption is associated with lower levels of coagulatory factors, but higher intake is associated with impaired fibrinolytic potential. These findings are consistent with the hypothesis that a balance between hemostatic and fibrinolytic activity may contribute to the complex relation of alcohol use with coronary heart disease.

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“…24 Mukamal et al 6 reported that higher intake of alcohol is associated with impaired fibrinolytic potentials. Thevananther and Brechen 25 have reported the direct action of acetaldehyde as a cause of the increase in the incidence of cardiovascular events associated with heavy drinking. Drinking has a diuretic action, promotes urination, and causes water imbalance, which eventually leads to dehydration that in turn will influence the renin-angiotensin-aldosterone system, increasing serum renin activity, angiotensin II and aldosterone.…”

Section: Influence Of Heavy Alcohol Consumptionmentioning

confidence: 99%

Effects of Alcohol Consumption on Cardiovascular Events in Male Patients With Healed Myocardial Infarction

Masunaga

Kimura

Miyataka

et al. 2006

Circ J

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Interaction of acetaldehyde with plasma proteins of the renin-angiotensin system

Cited by 30 publications

References 33 publications

Associations between aldehyde dehydrogenase 2 (ALDH2) genetic polymorphisms, drinking status, and hypertension risk in Japanese adult male workers: a case–control study

Associations between aldehyde dehydrogenase 2 (ALDH2) genetic polymorphisms, drinking status, and hypertension risk in Japanese adult male workers: a case–control study

Alcohol Consumption and Hemostatic Factors

Effects of Alcohol Consumption on Cardiovascular Events in Male Patients With Healed Myocardial Infarction

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