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Some studies suggest that lisinopril can reduce oxidative stress and improve lung function in the context of chronic alcohol ingestion, while other studies indicate that alcohol misuse may impair the effectiveness of lisinopril in treating hypertension.
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Lisinopril, an angiotensin-converting enzyme (ACE) inhibitor, is commonly prescribed for hypertension and heart failure. Alcohol consumption, particularly chronic abuse, can have significant effects on various bodily systems, including the cardiovascular and respiratory systems. This article explores the interactions between lisinopril and alcohol, focusing on their combined effects on oxidative stress, myocardial hypertrophy, and pulmonary function.
Chronic alcohol ingestion is known to increase oxidative stress in the lungs, leading to cellular dysfunction and increased risk of acute respiratory distress syndrome (ARDS). This oxidative stress is partly mediated by the activation of the renin-angiotensin system (RAS), which increases the production of superoxide and other reactive oxygen species (ROS) .
Lisinopril has been shown to attenuate the oxidative stress induced by chronic alcohol consumption. In a rat model, lisinopril treatment reduced the levels of glutathione disulfide and superoxide formation in the lung parenchyma, suggesting a protective effect against alcohol-induced oxidative damage. Additionally, lisinopril normalized the expression of transforming growth factor-beta1 (TGF-beta1) and improved alveolar epithelial barrier function, further highlighting its potential in mitigating alcohol-related pulmonary damage.
Chronic alcohol consumption can impair the regression of myocardial hypertrophy, even when treated with ACE inhibitors like lisinopril. In spontaneously hypertensive rats (SHR), alcohol ingestion reduced the effectiveness of lisinopril in decreasing left ventricular mass and protein content. This suggests that alcohol may interfere with the therapeutic effects of lisinopril on cardiac hypertrophy.
The study also found that alcohol+lisinopril rats had altered protein metabolism, with increased levels of myosin heavy chain compared to control+lisinopril rats. Additionally, the enzyme activities of proteases such as cathepsin D and dipeptidyl aminopeptidase I were not significantly increased in alcohol+lisinopril rats, indicating a compromised response to ACE inhibition in the presence of alcohol.
Lisinopril has been observed to decrease ethanol intake in rats. In a study where rats were given a sweetened alcoholic beverage, lisinopril administration led to a dose-related reduction in ethanol consumption while increasing water intake. This suggests that lisinopril may modulate the intake of alcohol, potentially through its effects on the RAS.
The interaction between lisinopril and alcohol is complex, involving multiple physiological pathways. While lisinopril can mitigate some of the oxidative stress and pulmonary damage induced by chronic alcohol consumption, its effectiveness in reducing myocardial hypertrophy may be compromised by alcohol. Additionally, lisinopril appears to reduce ethanol intake, which could have implications for managing alcohol abuse. These findings underscore the importance of considering alcohol consumption in patients undergoing ACE inhibitor therapy.
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