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一氧化氮在心脏疾病发病机制中的作用

Nitric oxide in the pathogenesis of cardiac disease.

作者信息

Raij Leopoldo

机构信息

Department of Medicine, Renal Division, and the Vascular Biology Institute, Miller School of Medicine, University of Miami, FL 33125-1624, USA.

出版信息

J Clin Hypertens (Greenwich). 2006 Dec;8(12 Suppl 4):30-9. doi: 10.1111/j.1524-6175.2006.06025.x.

DOI:10.1111/j.1524-6175.2006.06025.x
PMID:17170604
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8109667/
Abstract

Endothelial dysfunction is characterized by a vasoconstrictive and prothrombotic state in the vasculature; it plays a role in all stages of cardiac disease and is a significant independent predictor of cardiovascular outcomes. Nitric oxide (NO) performs multiple biologic activities in the endothelium, including vasodilation and antithrombotic actions. Reduced NO bioactivity is a major component of endothelial dysfunction. Impaired NO bioactivity is an important factor in the pathogenesis of atherosclerosis and in the metabolic syndrome. The functions of NO bioactivity in the heart go well beyond those in the endothelium, as all 3 NO synthase (NOS) isoforms-endothelial NOS, neuronal NOS, and inducible NOS-are expressed in cardiac myocytes and mediate systolic, diastolic, and chronotropic cardiac functions. Impairment of NO bioactivity is a pathogenic factor in various forms of cardiac disease. Although these findings support the potential use of NO-targeted therapies for treatment of cardiac disease, the complexities of the biologic actions of NO in the vasculature and heart are such that development of therapies is still largely in the preliminary stages.

摘要

内皮功能障碍的特征是血管系统处于血管收缩和促血栓形成状态;它在心脏病的各个阶段都起作用,并且是心血管结局的重要独立预测指标。一氧化氮(NO)在内皮中具有多种生物学活性,包括血管舒张和抗血栓作用。NO生物活性降低是内皮功能障碍的主要组成部分。NO生物活性受损是动脉粥样硬化发病机制和代谢综合征中的重要因素。NO生物活性在心脏中的功能远不止于内皮中的功能,因为所有三种NO合酶(NOS)同工型——内皮型NOS、神经元型NOS和诱导型NOS——都在心肌细胞中表达,并介导心脏的收缩、舒张和变时性功能。NO生物活性受损是各种形式心脏病的致病因素。尽管这些发现支持了针对NO的疗法在心脏病治疗中的潜在应用,但NO在血管系统和心脏中的生物学作用非常复杂,以至于疗法的开发仍主要处于初步阶段。

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