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Impact of the L-arginine-Nitric Oxide Pathway and Oxidative Stress on the Pathogenesis of the Metabolic Syndrome

机译:L-精氨酸一氧化氮途径和氧化应激对代谢综合征发病机制的影响。

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摘要

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.
机译:一氧化氮的生理作用的发现彻底改变了对血管紧张度,血小板粘附和聚集以及免疫激活的调节的认识。一氧化氮(NO)最引人入胜的方面可能是这种气体,在没有受体的情况下,可以调节正常的生理事件并在病理条件下介导细胞毒性。 NO合成酶(NOS)由L-精氨酸产生NO,生成L-瓜氨酸和NO。 L-精氨酸途径活性的调节发生在NO产生的水平。代谢综合征是一组胰岛素抵抗,血压升高和动脉粥样硬化血脂异常,这是心血管疾病的常见基础。它发生在具有环境影响的遗传易感人群中,并具有严重的经济和社会后果。药理学和非药理学治疗应个体化,并有针对性地使其血压,HDL胆固醇,甘油三酸酯和葡萄糖值的变化正常化。尽管在最近的几十年中,代谢综合征的患病率不断上升,但是在了解这种综合征的发病机理及其并发症的精确机制方面,进展甚微。越来越多的证据表明,NO,炎症和氧化应激在该综合征的生理病理中起重要作用。这篇综述总结并评估了L-精氨酸-NO途径和氧化应激在代谢综合征的生理病理学和系统性心血管事件中的参与,以及运动对这种综合征的影响。

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