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全球风险发病机制中的一氧化氮机制。

Nitric oxide mechanisms in the pathogenesis of global risk.

作者信息

Mason R Preston

机构信息

Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.

出版信息

J Clin Hypertens (Greenwich). 2006 Aug;8(8 Suppl 2):31-8; quiz 40. doi: 10.1111/j.1524-6175.2006.05838.x.

DOI:10.1111/j.1524-6175.2006.05838.x
PMID:16894246
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8109627/
Abstract

Identification and management of cardiovascular risk factors, such as hypertension, diabetes mellitus, and dyslipidemia, is essential not only for prevention of cardiovascular disease, but also for slowing the progression of existing cardiovascular disease. A major underlying mechanism that links various cardiovascular risk factors and manifestations of cardiovascular disease is endothelial dysfunction, characterized by impaired nitric oxide bioactivity. Oxidative stress is an important cause of impaired nitric oxide bioactivity, and a major pathogenic mechanism of atherosclerosis. Several pharmacologic therapies, including angiotensin-converting enzyme inhibitors, calcium channel blockers, statins, and the vasodilating beta blocker nebivolol, have been shown to enhance nitric oxide bioactivity and improve endothelial function. This effect may help explain the cardioprotective benefits of these agents and may stimulate further use of nitric oxide modulation for the treatment of cardiovascular risk factors and manifestations of cardiovascular disease.

摘要

识别和管理心血管危险因素,如高血压、糖尿病和血脂异常,不仅对于预防心血管疾病至关重要,而且对于减缓现有心血管疾病的进展也至关重要。连接各种心血管危险因素与心血管疾病表现的一个主要潜在机制是内皮功能障碍,其特征是一氧化氮生物活性受损。氧化应激是一氧化氮生物活性受损的重要原因,也是动脉粥样硬化的主要致病机制。包括血管紧张素转换酶抑制剂、钙通道阻滞剂、他汀类药物以及血管舒张性β受体阻滞剂奈必洛尔在内的几种药物治疗已被证明可增强一氧化氮生物活性并改善内皮功能。这种作用可能有助于解释这些药物的心脏保护益处,并可能促使进一步利用一氧化氮调节来治疗心血管危险因素和心血管疾病的表现。