Beta-Blockers and Oxidative Stress in Patients with Heart Failure

Pharmaceuticals
Kazufumi NakamuraHiroshi Ito

Abstract

Oxidative stress has been implicated in the pathogenesis of heart failure. Reactive oxygen species (ROS) are produced in the failing myocardium, and ROS cause hypertrophy, apoptosis/cell death and intracellular Ca(2+) overload in cardiac myocytes. ROS also cause damage to lipid cell membranes in the process of lipid peroxidation. In this process, several aldehydes, including 4-hydroxy-2-nonenal (HNE), are generated and the amount of HNE is increased in the human failing myocardium. HNE exacerbates the formation of ROS, especially H₂O₂ and ·OH, in cardiomyocytes and subsequently ROS cause intracellular Ca(2+) overload. Treatment with beta-blockers such as metoprolol, carvedilol and bisoprolol reduces the levels of oxidative stress, together with amelioration of heart failure. This reduction could be caused by several possible mechanisms. First, the beta-blocking effect is important, because catecholamines such as isoproterenol and norepinephrine induce oxidative stress in the myocardium. Second, anti-ischemic effects and negative chronotropic effects are also important. Furthermore, direct antioxidative effects of carvedilol contribute to the reduction of oxidative stress. Carvedilol inhibited HNE-induced intracellular Ca(2+) ov...Continue Reading

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Citations

Dec 12, 2012·Nihon yakurigaku zasshi. Folia pharmacologica Japonica·Kazufumi NakamuraHiroshi Ito
Jun 6, 2017·Journal of Veterinary Diagnostic Investigation : Official Publication of the American Association of Veterinary Laboratory Diagnosticians, Inc·Barbara VerkAleksandra Domanjko Petrič
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May 22, 2019·Journal of Molecular Histology·Cheng FanHaipeng Guo
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Apr 1, 2021·Acta Pharmacologica Sinica·Jie HuangHai-Yan Chen
May 6, 2021·Journal of Cellular and Molecular Medicine·Yaowen WangYuehui Yin

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Methods Mentioned

BETA
biopsy

Software Mentioned

COMET
MUCHA

Related Concepts

Related Feeds

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis