ArticleJournal of physiology and biochemistry2014
Acute ethanol intake induces mitogen-activated protein kinase activation, platelet-derived growth factor receptor phosphorylation, and oxidative stress in resistance arteries.
Article in Journal of physiology and biochemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 49 citations in OpenAlex.
- Mineralocorticoid receptors are implicated in the initial steps of the cardiorenal damage induced by ethanol.Frontiers in cardiovascular medicine · 2026Article
- Ethanol-induced dysfunction of the mesenteric perivascular adipose tissue is driven by mineralocorticoid receptors.Pflugers Archiv : European journal of physiology · 2025Article
- Alcohol consumption may be a risk factor for cerebrovascular stenosis in acute ischemic stroke and transient ischemic attack.BMC neurology · 2024Article
- Reactive oxygen species (ROS) scavenging biomaterials for anti-inflammatory diseases: from mechanism to therapy.Journal of hematology & oncology · 2023Review
- Gut Microbiota: Target for Modulation of Gut-Liver-Adipose Tissue Axis in Ethanol-Induced Liver Disease.Mediators of inflammation · 2022Review
- Nebivolol Prevents Up-Regulation of Nox2/NADPH Oxidase and Lipoperoxidation in the Early Stages of Ethanol-Induced Cardiac Toxicity.Cardiovascular toxicology · 2021Article
- Tetrahydrobiopterin Restores Microvascular Dysfunction in Young Adult Binge Drinkers.Alcoholism, clinical and experimental research · 2020Article
- Increased mitochondrial ROS generation mediates the loss of the anti-contractile effects of perivascular adipose tissue in high-fat diet obese mice.British journal of pharmacology · 2017Article
- Cardiovascular Consequences of Binge Drinking: An Integrative Review with Implications for Advocacy, Policy, and Research.Alcoholism, clinical and experimental research · 2017Review
- Reactive oxygen species derived from NAD(P)H oxidase play a role on ethanol-induced hypertension and endothelial dysfunction in rat resistance arteries.Journal of physiology and biochemistry · 2017Article
- Acute Ethanol Intake Induces NAD(P)H Oxidase Activation and Rhoa Translocation in Resistance Arteries.Arquivos brasileiros de cardiologia · 2016Article
- Relative Role of Akt, ERK and CREB in Alcohol-Induced Microglia P2X4R Receptor Expression.Alcohol and alcoholism (Oxford, Oxfordshire) · 2016Article
- The protective effect of lipoic acid on selected cardiovascular diseases caused by age-related oxidative stress.Oxidative medicine and cellular longevity · 2015Review
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
In the present study, we investigated the role of angiotensin type I (AT1) receptor in reactive oxygen species (ROS) generation and mitogen-activated protein kinases (MAPK) activation induced by acute ethanol intake in resistance arteries. We also evaluated the effect of ethanol on platelet-derived growth factor receptors (PDGF-R) phosphorylation and the role of this receptor on ROS generation by ethanol. Ethanol (1 g/kg; p.o. gavage) effects were assessed within 30 min in male Wistar rats. Acute ethanol intake did not alter angiotensin I or angiotensin II levels in the rat mesenteric arterial bed (MAB). Ethanol induced vascular oxidative stress, and this response was not prevented by losartan (10 mg/kg; p.o. gavage), a selective AT1 receptor antagonist. MAB from ethanol-treated rats displayed increased SAPK/JNK and PDGF-R phosphorylation, responses that were not prevented by losartan. The phosphorylation levels of protein kinase B (Akt) and eNOS were not affected by acute ethanol intake. MAB nitrate levels and the reactivity of this tissue to acetylcholine, phenylephrine, and sodium nitroprusside were not affected by ethanol intake. Ethanol did not alter plasma antioxidant capacity, the levels of reduced glutathione, or the activities of superoxide dismutase and catalase in the rat MAB. Short-term effects of ethanol (50 mmol/l) were evaluated in vascular smooth muscle cells (VSMC) isolated from rat MAB. Ethanol increased ROS generation, and this response was not affected by AG1296, a PDGF-R inhibitor, or losartan. Finally, ethanol did not alter MAPK or PDGF-R phosphorylation in cultured VSMC. Our study provides novel evidence that acute ethanol intake induces ROS generation, PDGF-R phosphorylation, and MAPK activation through AT(1)-independent mechanisms in resistance arteries in vivo. MAPK and PDGF-R play a role in vascular signaling and cardiovascular diseases and may contribute to the vascular pathobiology of ethanol.
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