Losartan and alcohol interaction
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Losartan and Alcohol Interaction: Cardiovascular and Vascular Effects
Alcohol, the Renin-Angiotensin System, and Vascular Dysfunction
Alcohol consumption, especially in excess, is linked to increased cardiovascular risk, partly through activation of the renin-angiotensin system (RAS) and its downstream effects. Ethanol can trigger the angiotensin II (Ang II) pathway, leading to vascular dysfunction by increasing oxidative stress and mitochondrial dysfunction in blood vessels. This process results in higher production of mitochondrial reactive oxygen species (mtROS), reduced nitric oxide (NO) and hydrogen peroxide (H2O2) bioavailability, and ultimately, vascular hypercontractility and endothelial dysfunction. Losartan, an angiotensin II type 1 receptor (AT1R) blocker, has been shown to prevent these ethanol-induced vascular changes, restoring mitochondrial function and antioxidant defenses in animal models Awata2023Awata2023Ceron2017.
Losartan’s Protective Role Against Alcohol-Induced Cardiovascular Damage
Multiple studies demonstrate that losartan can counteract the harmful cardiovascular effects of alcohol. In animal models, losartan prevented ethanol-induced increases in vascular contractility, oxidative stress, and changes in protein expression related to vascular health. It also protected against mitochondrial dysfunction and restored antioxidant enzyme levels, such as SOD2, in the aorta Awata2023Awata2023Ceron2017. In human cell models, losartan protected heart muscle cells from alcohol-induced oxidative stress and damage, likely by blocking the Ang II/AT1R pathway and reducing NOX enzyme activity, which is involved in oxidative stress .
Alcohol, Losartan, and Blood Pressure Control in Hypertensive Patients
In clinical studies involving hypertensive patients with left ventricular hypertrophy, moderate alcohol consumption did not interfere with the blood pressure-lowering or stroke risk reduction benefits of losartan compared to another antihypertensive, atenolol. However, high alcohol intake tended to increase stroke risk, even though it reduced the risk of myocardial infarction. Importantly, there was no significant interaction between alcohol consumption and losartan’s effectiveness in reducing cardiovascular events .
Losartan and Alcohol-Induced Kidney and Heart Injury
Chronic alcohol intake can cause kidney damage and fibrosis, as well as heart muscle injury. Losartan has been shown to reduce markers of kidney injury, inflammation, and fibrosis in animal models exposed to alcohol, likely by modulating fibrotic and inflammatory pathways . In heart cells, losartan reduced alcohol-induced oxidative stress and protected against cardiotoxicity .
Losartan and Acute Alcohol Effects
Losartan may also reduce some of the acute intoxicating effects of low doses of alcohol in animal studies, possibly by blocking Ang II-mediated pathways in the brain. However, this effect is less pronounced at higher alcohol doses . In models of acute alcohol-induced increases in pulmonary arterial pressure, losartan partially prevented vascular remodeling and oxidative stress, though it did not fully block the pressure increase .
Losartan and Cognitive Effects in Prenatal Alcohol Exposure
In a mouse model of prenatal alcohol exposure, losartan did not cause developmental harm and improved learning and memory in control animals. However, it did not significantly improve cognitive outcomes in alcohol-exposed offspring, with some sex-specific differences observed .
Conclusion
Overall, research indicates that losartan can protect against many of the harmful cardiovascular, vascular, and kidney effects of alcohol by blocking the Ang II/AT1R pathway and reducing oxidative stress. Losartan does not appear to negatively interact with alcohol in terms of blood pressure control or cardiovascular event reduction in hypertensive patients. However, high alcohol intake still poses significant health risks, and losartan’s protective effects may not extend to all organ systems or all types of alcohol-induced damage.
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Most relevant research papers on this topic
Vascular injury associated with ethanol intake is driven by AT1 receptor and mitochondrial dysfunction
Ethanol-induced vascular dysfunction is driven by AT1 receptor and mitochondrial dysfunction, with losartan effectively preventing these effects and restoring SOD2 expression.
Ethanol induces endothelial dysfunction via angiotensin II: Role of mitochondrial ROS
Ethanol consumption leads to endothelial dysfunction by increasing angiotensin II levels, triggering mitochondria dysfunction, and increasing reactive oxygen species production, with losartan treatment potentially preventing this effect.
Data on the effects of losartan on protein expression, vascular reactivity and antioxidant capacity in the aorta of ethanol-treated rats
Losartan protects against ethanol-induced oxidative stress and vascular reactivity in rats, while ethanol and losartan do not affect endothelium-dependent relaxation.
Losartan protects human stem cell-derived cardiomyocytes from angiotensin II-induced alcoholic cardiotoxicity
Losartan protects human stem cell-derived cardiomyocytes from angiotensin II-induced alcoholic cardiotoxicity, potentially by regulating oxidative stress damage through NOX regulation.
Losartan reduces ethanol intoxication in the rat.
Losartan effectively reduces the intoxicating effects of low doses of ethanol in rats, but not the higher doses, suggesting higher doses may be more difficult to block due to direct effects on the post synaptic membrane.
Metformin versus losartan: prevention of non-alcoholic fatty liver disease in adult albino rats, an immunohistochemical study.
Metformin and losartan effectively prevent non-alcoholic fatty liver disease in rats, with both drugs partially preserving hepatic architecture.
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