C R Assumpção, T M C Brunini, C Matsuura, A C Resende, A C Mendes-Ribeiro
Departamento de Farmacologia e Psicobiologia, Instituto de Biologia, Av. 28 de Setembro 87 CEP 20551-030, Rio de Janeiro, Brazil.
Open Biochem J. 2008;2:108-15. doi: 10.2174/1874091X00802010108. Epub 2008 Jul 14.
The discovery of the physiological roles of nitric oxide has revolutionized the understanding of regulation of vascular tone, platelet adhesion and aggregation, and immune activation. Perhaps the most intriguing aspect of nitric oxide (NO) is that it is a gas that, in the absence of receptors, can regulate both normal physiological events and mediate cytotoxicity under pathological conditions. NO is produced from L-arginine by NO synthases (NOS), yielding L-citrulline and NO. The regulation of L-arginine pathway activity occurs at the level of NO production. The metabolic syndrome is a cluster of insulin resistance, elevated blood pressure, and atherogenic dyslipidemia, a common basis of cardiovascular disease. It occurs in genetically susceptible individuals with environmental influences and has serious economic and social consequences. Pharmacological and non-pharmacological therapies should be individualized and targeted to normalize its alterations of blood pressure, HDL cholesterol, triglycerides and glucose values. Despite the increasing prevalence of the metabolic syndrome in the last decades, there has been little progress in the understanding of the precise mechanisms involved in the pathogenesis of this syndrome and its complications. Emerging evidence is available that NO, inflammation and oxidative stress play important roles in the physiopathology of this syndrome. This review summarizes and evaluates the participation of the L-arginine-NO pathway and oxidative stress in the physiopathology of the metabolic syndrome and cardiovascular events at the systemic level, as well as the effects of exercise on this syndrome.
一氧化氮生理作用的发现彻底改变了人们对血管张力调节、血小板黏附和聚集以及免疫激活的理解。一氧化氮（NO）最引人入胜的方面或许在于它是一种气体，在没有受体的情况下，既能调节正常生理活动，又能在病理条件下介导细胞毒性。NO由一氧化氮合酶（NOS）作用于L-精氨酸产生，生成L-瓜氨酸和NO。L-精氨酸途径活性的调节发生在NO生成水平。代谢综合征是一组包括胰岛素抵抗、血压升高和致动脉粥样硬化血脂异常的症候群，是心血管疾病的常见基础。它发生在受环境影响的遗传易感个体中，具有严重的经济和社会后果。药物和非药物治疗应个体化，并旨在使血压、高密度脂蛋白胆固醇、甘油三酯和血糖值的改变恢复正常。尽管在过去几十年中代谢综合征的患病率不断上升，但在理解该综合征及其并发症发病机制所涉及的精确机制方面进展甚微。现有新证据表明，NO、炎症和氧化应激在该综合征的病理生理学中起重要作用。本综述总结并评估了L-精氨酸-NO途径和氧化应激在代谢综合征和全身心血管事件病理生理学中的参与情况，以及运动对该综合征的影响。
