Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Reactive oxygen species are central mediators of vascular dysfunction and hypertension induced by ethanol consumption

Version 1 : Received: 6 September 2023 / Approved: 6 September 2023 / Online: 7 September 2023 (11:00:10 CEST)

A peer-reviewed article of this Preprint also exists.

Padovan, J.C.; Dourado, T.M.H.; Pimenta, G.F.; Bruder-Nascimento, T.; Tirapelli, C.R. Reactive Oxygen Species Are Central Mediators of Vascular Dysfunction and Hypertension Induced by Ethanol Consumption. Antioxidants 2023, 12, 1813. Padovan, J.C.; Dourado, T.M.H.; Pimenta, G.F.; Bruder-Nascimento, T.; Tirapelli, C.R. Reactive Oxygen Species Are Central Mediators of Vascular Dysfunction and Hypertension Induced by Ethanol Consumption. Antioxidants 2023, 12, 1813.

Abstract

Consumption of high amounts of ethanol is a risk factor for development of cardiovascular diseases such as arterial hypertension. The hypertensive state induced by ethanol is a complex multi-factorial event, and oxidative stress is a pathophysiological hallmark of vascular dysfunction associated with ethanol consumption. Increasing levels of reactive oxygen species (ROS) in the vasculature triggers important processes underlying vascular injury, including accumulation of intracellular Ca2+ ions, reduced bioavailability of nitric oxide (NO), activation of mitogen-activated protein kinases (MAPKs), endothelial dysfunction, and loss of the anticontractile effect of perivascular adipose tissue (PVAT). The enzyme nicotinamide adenine dinucleotide phosphate (NADPH) oxidase plays a central role in vascular ROS generation in response to ethanol. Activation of the renin-angiotensin-aldosterone system (RAAS) is an upstream mechanism which contributes to NADPH oxidase stimulation, overproduction of ROS and vascular dysfunction. This review discusses the mechanisms of vascular dysfunction induced by ethanol, detailing the contribution of ROS to these processes. Data examining the association between neuroendocrine changes and vascular oxidative stress induced by ethanol are also reviewed and discussed. These issues are of paramount interest to public health as ethanol contributes to blood pressure elevation in the general population, and it is linked to cardiovascular conditions and diseases.

Keywords

Oxidative stress; NADPH oxidase; Ethanol; Blood pressure; Endothelium

Subject

Biology and Life Sciences, Other

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