Mild but prolonged elevation of serum angiotensin converting enzyme (ACE) activity in alcoholics

Okuno, Fumio; Arai, Michitsugu; Ishii, Hiromi; Shigeta, Yohsuke; Ebihara, Yoshinori; Takagi, Satoshi; Tsuchiya, Masayuki

doi:10.1016/0741-8329(86)90053-4

Cited by 28 publications

(23 citation statements)

References 12 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%

“…7 Alcoholics also have enhanced serum ACE activity. 9 The early RAS activation in the present study may have been caused by a direct effect of alcohol on the RAS or through an alcohol-induced reduction of plasma volume, a reduction in blood pressure, an alteration in sodium balance or sympathetic activation, and/or by production of cardiac depression and cardiac hemodynamic overload (including increased LV wall stress). 23 It is evident that myocardial stretch and/or the increase in shortening load on the myocardium turns on the genes of the RAS.…”

Section: Ras Activation and Chronic At 1 Receptor Blockadementioning

confidence: 92%

See 1 more Smart Citation

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%

Section: Ras Activation and Chronic At 1 Receptor Blockadementioning

confidence: 92%

Angiotensin II Type 1 Receptor Blockade Prevents Alcoholic Cardiomyopathy

Cheng

Cunningham

et al. 2006

Circulation

View full text Add to dashboard Cite

show abstract

“…The association of serum y-GTP with blood pressure elevations in alcohol consumers was also suggested to be a reflection of hepatic cell damage rather than enzyme induction, since serum angiotensin-converting enzyme (ACE), which is elevated in alcoholic liver disease but not induced in the liver cells (12,13), also showed an association with blood pressure in alcohol consumers (14). The hepatic cell damage must be related to hepatic steatosis since it is the earliest liver manifestation in alcohol consumers (15,16).…”

mentioning

confidence: 99%

The Relationship between Serum Gamma-Glutamyl Transpeptidase Levels and Hypertension: Common in Drinkers and Nondrinkers.

et al. 1995

View full text Add to dashboard Cite

A significant association between elevations of serum gamma-glutamyl transpeptidase (y-GTP) levels and those of blood pressure and hypertension has been reported separately in drinkers and nondrinkers. The aim of the present study is to evaluate whether the relationship between serum y-GTP and the prevalence of hypertension is the same or similar in both drinkers and nondrinkers. The study subjects comprised 4,920 male nondrinkers, 9,390 male daily drinkers, 8,081 female nondrinkers, and 278 female daily drinkers, who were aged 40 to 59 years. The prevalence of hypertension in the male and female daily drinkers was 1.5 and 1.3 times, respectively, higher than in the nondrinkers. Mean systolic blood pressure in the male and female drinkers was 4.4 and 3.1 mmHg, respectively, higher than in the nondrinkers. After adjusting for age, body mass index, and serum y-GTP levels, the differences in the prevalence of hypertension and the mean systolic blood pressure level between the drinkers and nondrinkers decreased to 1.2 times and 2.7 mmHg, respectively. Although these small differences remained statistically significant, the association between serum y-GTP and hypertension appears to be quite similar in both drinkers and nondrinkers, suggesting that hepatic steatosis may play a common, pathogenetic role in the development of hypertension. (Hypertens Res 1995; 18: 295-301)

show abstract

“…It forms through the cleavage of angiotensinogen by renin and angiotensin converting enzyme (ACE) and acquires functionality by binding to AT1R or Ang II type 2 receptors. Studies have shown that alcoholics exhibit increased plasma renin activity and serum ACE activity, which enhance RAS activation and increase Ang II levels . Furthermore, the upregulated mRNA levels and activity in the cardiac angiotensinogen‐ACE‐Ang I‐Ang II‐renin cascade, which can be inhibited by an angiotensin receptor blocker, have been reported in chronic alcohol‐fed rats .…”

Section: Discussionmentioning

confidence: 99%