Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2020;16(3):181-191.
doi: 10.2174/1573402115666190325124622.

Ethanol Induced Oxidative Stress in the Vasculature: Friend or Foe

Shane A Phillips  1 , Kendra Osborn  2 , Chueh-Lung Hwang  1 , Ahmad Sabbahi  1 , Mariann R Piano  2
Affiliations
Review

Ethanol Induced Oxidative Stress in the Vasculature: Friend or Foe

Shane A Phillips et al. Curr Hypertens Rev. 2020.

Abstract

Oxidative stress is implicated in the etiology of many ethanol-induced pathologies. Oxidative stress has been shown to contribute to the development of endothelial dysfunction and cardiovascular disease, such as hypertension. This review details mechanisms of vascular function, the role of oxidative stress in vascular biology and how ethanol consumption may alter endothelial and smooth muscle cell function as well as microvascular function. Also reviewed are data from human investigations that have examined the association between alcohol consumption and changes in blood pressure and increased risk for hypertension.

Keywords: Alcohol; ethanol-induced pathologies; hypertension; microvascular function.; oxidative stress; vasculature.

PubMed Disclaimer

Figures

Figure 1.
Figure 1.
Endothelial cell-derived vasodilators and constrictors. ANGII, angiotensin II; AT1, ANGII receptor type 1; AT2, ANGII receptor type 2; BH4, tetrahydrobiopterin; Ca2+, calcium; Cav-1, caveolin-1; CaM, calmodulin; COX, cyclooxygenases; Cyp450, cytochrome p450; EET, epoxyeicosatrienoic acids; eNOS, endothelial nitric oxide synthase; ETA, endothelin receptors type A; ETB, endothelin receptors type B; ET-1, endothelin-1; H2O2, hydrogen peroxide; NADPH, nicotinamide adenine dinucleotide phosphate; NO, nitric oxide; O2•, superoxide; PGI2, prostacyclin; PI3K, phosphotidylinositol-3-kinase; PDK1, phosphoinositide-dependent kinase-1; SOD, superoxide dismutase; TXA2, thromboxane A2.
Figure 2.
Figure 2.
Summary of the pro oxidant effects of alcohol on the mechanisms of vascular relaxation and constriction. ADH, alcohol dehydrogenase; ANGII, angiotensin II; BH4, tetrahydrobiopterin; CYP2E1, cytochrome P450 2E1; eNOS, endothelial nitric oxide synthase; ET-1, endothelin-1; FAEE, fatty acid ethyl ester; H2O2, hydrogen peroxide; NADH/NAD+, nicotinamide adenine dinucleotide reduced/ nicotinamide adenine dinucleotide; NADPH, nicotinamide adenine dinucleotide phosphate; NO, nitric oxide; O2•, superoxide; PLD, phospholipase D; ROS, reactive oxygen species; SOD, superoxide dismutase.
See this image and copyright information in PMC

References

    1. Piano MR, Phillips SA. Alcoholic cardiomyopathy: pathophysiologic insights. Cardiovasc Toxicol. 2014;14(4):291–308. - PMC - PubMed
    1. Fernandez-Checa JC, Kaplowitz N, Garcia-Ruiz C, Colell A. Mitochondrial glutathione: importance and transport. Seminars in liver disease. 1998;18(4):389–401. - PubMed
    1. Zhu H, Jia Z, Misra H, Li YR. Oxidative stress and redox signaling mechanisms of alcoholic liver disease: updated experimental and clinical evidence. J Dig Dis. 2012;13(3):133–42. - PMC - PubMed
    1. Landmesser U, Harrison DG. Oxidative stress and vascular damage in hypertension. CoronArtery Dis. 2001;12(6):455–61. - PubMed
    1. Jonk AM, Houben AJ, de Jongh RT, Serne EH, Schaper NC, Stehouwer CD. Microvascular dysfunction in obesity: a potential mechanism in the pathogenesis of obesity-associated insulin resistance and hypertension. Physiology(Bethesda). 2007;22:252–60. - PubMed

Publication types