Hypertension and cardiovascular risk factors - Role of the angiotensin II-nitric oxide interaction
Hypertension and cardiovascular risk factors - Role of the angiotensin II-nitric oxide interaction
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DOI：
10.1161/01.hyp.37.2.767
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发表时间：
2001-02-01
期刊：
影响因子：
8.3
通讯作者：
Raij, L
中科院分区：
文献类型：
--
作者：
Raij, L
血管一氧化氮（NO）的上调是对血压升高的适应性反应，可能有助于预防终末器官损伤。高血压患者心血管和肾脏发病率和死亡率的差异可能至少部分是由于高血压血流动力学负荷引起的内皮功能个体差异。在正常情况下，血管紧张素（Ang）II和NO之间存在功能反馈平衡。NO-Ang II失衡可能不能解释高血压的所有血管病理生理学，但它肯定是一个重要组成部分。在高血压中，盐敏感性，是否原发（即美国和日本的某些人群）或中学（即，衰老，II型糖尿病），似乎是心血管和肾脏风险增加的标志，通常与NO生物活性降低有关。在糖尿病和动脉粥样硬化中，NO依赖性血管舒张受损，并可通过减少合成和/或阻断Ang II的作用来恢复。对高血压、心血管危险因素、终末器官损伤和NO-Ang II轴之间的关系的理解使人们相信，能够恢复血管壁内这些血管活性分子的稳态平衡的治疗剂的组合将是预防或阻止终末器官疾病最有效的。
Vascular upregulation of nitric oxide (NO) is an adaptive response to increased blood pressure that may help in the prevention of end-organ damage. Differences in cardiovascular and renal morbidity and mortality in hypertensive patients may result, at least in part, from individual variations in endothelial function in response to the hemodynamic workload of hypertension. A functional feedback balance exists between both angiotensin (Ang) II and NO under normal conditions. The NO-Ang II imbalance may not explain all the vascular pathophysiology of hypertension, but it certainly appears to be an important component. In hypertension, salt sensitivity, whether primary (ie, certain populations in the United States and Japan) or secondary (ie, aging, type II diabetes), appears to be a marker of increased cardiovascular and renal risk that is often linked to a decreased bioactivity of NO. In diabetes and atherosclerosis, NO-dependent vascular relaxation is impaired and can be restored by decreasing the synthesis and/or blocking the action of Ang II. An understanding of the relations between hypertension, cardiovascular risk factors, end-organ damage, and the NO-Ang II axis leads one to believe that the combination of therapeutic agents capable of reinstating the homeostatic balance of these vasoactive molecules within the vessel wall would be most effective in preventing or arresting end-organ disease.