Jin Richard C, Loscalzo Joseph
Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
J Blood Med. 2010 Aug 1;2010(1):147-162. doi: 10.2147/JBM.S7000.
Nitric oxide (NO) is a structurally simple, highly versatile molecule that was originally discovered over 30 years ago as an endothelium-derived relaxing factor. In addition to its vasorelaxing effects, NO is now recognized a key determinant of vascular health, exerting antiplatelet, antithrombotic, and anti-inflammatory properties within the vasculature. This short-lived molecule exerts its inhibitory effect on platelets largely through cGMP-dependent mechanisms, resulting in a multitude of molecular effects by which platelet activation and aggregation are prevented. The biosynthesis of NO occurs via the catalytic activity of nitric oxide synthase (NOS), an oxido-reductase found in many cell types. Nitric oxide insufficiency can be attributed to limited substrate/cofactor availability as well as interactions with reactive oxygen species (ROS). Impaired NO bioavailability represents the central feature of endothelial dysfunction, a common abnormality found in many vascular diseases. In this review, we present an overview of NO synthesis and biochemistry, discuss the mechanisms of action of NO in regulating platelet and endothelial function, and review the effects of vascular disease states on NO bioavailability.
一氧化氮（NO）是一种结构简单、功能多样的分子，30多年前最初被发现是一种内皮衍生的舒张因子。除了其血管舒张作用外，NO现在被认为是血管健康的关键决定因素，在血管系统中发挥抗血小板、抗血栓形成和抗炎特性。这种寿命短暂的分子主要通过依赖环磷酸鸟苷（cGMP）的机制对血小板发挥抑制作用，从而产生多种分子效应，防止血小板活化和聚集。NO的生物合成通过一氧化氮合酶（NOS）的催化活性发生，NOS是一种在许多细胞类型中发现的氧化还原酶。一氧化氮不足可归因于底物/辅助因子可用性有限以及与活性氧（ROS）的相互作用。NO生物利用度受损是内皮功能障碍的核心特征，内皮功能障碍是许多血管疾病中常见的异常情况。在本综述中，我们概述了NO的合成和生物化学，讨论了NO调节血小板和内皮功能的作用机制，并综述了血管疾病状态对NO生物利用度的影响。
