Nitric Oxide and Oxidative Stress-Mediated Cardiovascular Functionality: From Molecular Mechanism to Cardiovascular Disease

Weilue He, M. Kwesiga, Eyerusalem A Gebreyesus, Sijia Liu
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引用次数: 10

Abstract

The underlying pathology of most cardiovascular diseases (CVDs) such as coronary artery disease, high blood pressure, and stroke involves decreased cardiovascular contractility and anatomic alterations in cardiovascular structures. Nitric oxide (NO) regulates vascular tone and contractile function of myocardium and maintains blood vessel homeostasis. Interestingly, the effect of NO is like a double-edged sword in the body. Insufficient NO causes hypertension and atherosclerosis, while an overproduction of NO may foster inflammation and cause heart infarction and shock. In addition, growing evidences have shown that oxidative stress plays pivotal roles in the initiation and progression of CVDs. This chapter will discuss in detail the roles NO plays in the cardiovascular system under both physiological and pathological conditions. We will focus on: (1) the molecular mechanism of cardiovascular contraction, (2) NO/Ca2+-induced muscle relaxation, (3) NO-related structural change in blood vessels, and (4) redox balance in the cardiovascular system. The relationships between these molecular mechanisms and the characteristics of CVDs will be highlighted.
一氧化氮和氧化应激介导的心血管功能:从分子机制到心血管疾病
大多数心血管疾病(cvd)如冠状动脉疾病、高血压和中风的潜在病理涉及心血管收缩能力下降和心血管结构的解剖改变。一氧化氮(NO)调节血管张力和心肌收缩功能,维持血管稳态。有趣的是,一氧化氮在体内的作用就像一把双刃剑。一氧化氮不足可引起高血压和动脉粥样硬化,而一氧化氮过量可引起炎症,引起心肌梗死和休克。此外,越来越多的证据表明,氧化应激在心血管疾病的发生和发展中起着关键作用。本章将详细讨论一氧化氮在生理和病理条件下在心血管系统中的作用。我们将重点关注:(1)心血管收缩的分子机制,(2)NO/Ca2+诱导的肌肉松弛,(3)NO相关的血管结构变化,以及(4)心血管系统的氧化还原平衡。本文将重点讨论这些分子机制与cvd特性之间的关系。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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