Reactive Oxygen Species Are Central Mediators of Vascular Dysfunction and Hypertension Induced by Ethanol Consumption

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 trigger 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.

Diet and risk of temporomandibular disorders: a Mendelian randomization study

“…This study identi ed a correlation between alcoholic drinks per week intake and the risk of developing TMD. This nding is consistent with that reported by Miettinen et al who demonstrated a signi cant association between alcohol consumption and TMD symptoms among young adults in Finland [19]. Alcohol consumption's close relationship to TMD is mainly attributed to the pathological effects of alcohol on the human body in many aspects.…”

Taurine Prevents Angiotensin II-Induced Human Endocardial Endothelium Morphological Remodeling and the Increase in Cytosolic and Nuclear Calcium and ROS

“…This circulating factor is produced mainly by the brain and the heart. Nutrients, particularly seafood [ 21 , 22 , 23 , 24 , 25 , 26 ], ensure its supplementation. Taurine’s beneficial effects are numerous, particularly at the cardiovascular level.…”

“…We took into consideration the following: 1—Ang II induces cardiac hypertrophy associated with an increase in cardiomyocyte intracellular Ca 2+ and ROS [ 15 ]; 2—the first abnormal remodeling takes place at the EE during the development of hereditary cardiomyopathy, and it contributes to cardiovascular dysfunction [ 21 ]; 3—endothelial cell dysfunction is a complex mechanism [ 29 ] implicating ROS generation and overload that is also activated by Ang II [ 22 , 23 , 24 , 25 ]. Thus, in the present study, we wanted to verify whether Ang II induces hypertrophy of human EECs and whether this effect can be prevented by treatment with taurine.…”