Elevations in plasma angiotensin II with prolonged ethanol treatment in rats

Wright, John W.; Morseth, Sandra L.; Abhold, Raymond H.; Harding, Joseph W.

doi:10.1016/0091-3057(86)90416-8

Cited by 66 publications

(41 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the present study and consistent with past reports, 1,6,7,9,23,24 chronic alcohol ingestion was accompanied by a similar profile of RAS activation. However, contrary to heart failure due to other causes, changes in RAS occurred early in the course of chronic alcohol consumption.…”

Section: Ras Activation and Chronic At 1 Receptor Blockadesupporting

confidence: 82%

Angiotensin II Type 1 Receptor Blockade Prevents Alcoholic Cardiomyopathy

Cheng

Cunningham

et al. 2006

Circulation

View full text Add to dashboard Cite

Background-Activation of the renin-angiotensin system (RAS) may contribute to the development of alcoholic cardiomyopathy. We evaluated the effect of angiotensin II (Ang II) type 1 receptor (AT 1 ) blockade on the development of alcoholic cardiomyopathy. Methods and Results-We serially evaluated left ventricular (LV) and cardiomyocyte function and the RAS over 6 months in 3 groups of instrumented dogs. Eight animals received alcohol (once per day orally, providing 33% of total daily caloric intake); 6 received alcohol and irbesartan (5 mg · kg Ϫ1 · d Ϫ1 PO); and 8 were controls. Compared with controls, alcohol ingestion caused sustained RAS activation with progressive increases in plasma levels of Ang II, renin activity, LV angiotensin-converting enzyme activity, and LV myocyte Ang II AT 1 receptor expression. The RAS activation was followed by a progressive fall in LV contractility (E ES , alcohol-fed dogs 3.9Ϯ0.

show abstract

Section: Ras Activation and Chronic At 1 Receptor Blockadesupporting

confidence: 82%

Angiotensin II Type 1 Receptor Blockade Prevents Alcoholic Cardiomyopathy

Cheng

Cunningham

et al. 2006

Circulation

View full text Add to dashboard Cite

show abstract

“…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

View full text Add to dashboard Cite

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

show abstract

“…While alcohol undoubtedly predisposes to ARDS through many mechanisms, oxidative stress is a key factor (4-7). Chronic alcohol ingestion reduces the level of the antioxidant glutathione (GSH) in bronchoalveolar lavage (BAL) fluid (8) and increases renin-angiotensin system (RAS) activity (9)(10)(11).…”

mentioning

confidence: 99%

Chronic Ethanol Ingestion Increases Superoxide Production and NADPH Oxidase Expression in the Lung

Polikandriotis

Rupnow

Elms

et al. 2006

Am J Respir Cell Mol Biol

View full text Add to dashboard Cite

Alcohol abuse increases the incidence of acute respiratory distress syndrome and causes oxidative stress and cellular dysfunction in the lung. The mechanisms of ethanol (EtOH)-induced oxidative stress in the lung remain to be defined. Chronic alcohol ingestion has been associated with increased renin-angiotensin system (RAS) activity. Therefore, the current study investigated the ability of lisinopril, an angiotensin-converting enzyme (ACE) inhibitor, to modulate oxidative stress in the lung after chronic EtOH ingestion in a well-established rat model. Male Sprague-Dawley rats were fed liquid diets containing EtOH (36% of calories) or maltose-dextrin as an isocaloric substitution for EtOH (Control) for 6 wk. Selected animals were also treated with lisinopril (3 mg/liter) for 6 wk. Chronic EtOH ingestion increased bronchoalveolar lavage fluid glutathione disulfide levels and superoxide formation in lung parenchyma. These effects of EtOH were attenuated by lisinopril treatment. Chronic EtOH ingestion failed to increase ACE expression or angiotensin II levels in lung homogenates, but increased angiotensinogen, angiotensin II type 1 and type 2 receptor levels, and ACE activity. Chronic EtOH ingestion also increased the levels of the NADPH oxidase subunit, gp91phox, an effect that was attenuated by lisinopril, but had no effect on lung p22phox or p47phox levels. These findings suggest that EtOH-mediated RAS activation plays an important role in pulmonary oxidative stress and provide new insights into mechanisms by which EtOH causes oxidative stress in the lung and potential strategies of lung protection through ACE inhibition. Keywords: ARDS; chronic ethanol ingestion; lung; NADPH oxidase; superoxideThe acute respiratory distress syndrome (ARDS) is a severe form of lung injury characterized by noncardiogenic pulmonary edema in response to diverse clinical scenarios such as sepsis, trauma, or aspiration that cause systemic activation of proinflammatory cascades (1). Despite extensive research, ARDS is associated with a 50% mortality rate, due in part to the lack of effective therapies (2). Therefore, identifying mechanisms that predispose the lung to acute injury has the potential to further our understanding of ARDS pathophysiology and the design of

show abstract

Elevations in plasma angiotensin II with prolonged ethanol treatment in rats

Cited by 66 publications

References 31 publications

Angiotensin II Type 1 Receptor Blockade Prevents Alcoholic Cardiomyopathy

Angiotensin II Type 1 Receptor Blockade Prevents Alcoholic Cardiomyopathy

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

Chronic Ethanol Ingestion Increases Superoxide Production and NADPH Oxidase Expression in the Lung

Contact Info

Product

Resources

About