Oxidative stress in essential hypertension.

Oxidative stress in essential hypertension.
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原发性高血压的氧化应激。

DOI:
10.2174/1381612043384619
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发表时间:
2004
影响因子:
3.1
通讯作者:
Roberto Manfredini
Roberto Manfredini
中科院分区:
医学4区
文献类型:
--
作者:
Francesco Portaluppi;B. Boari;Roberto Manfredini

文献摘要

被引文献

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原发性高血压内皮功能障碍的一个主要原因是一氧化氮(NO)的可用性降低。NO生物利用度的损害可能是影响NO合成以及NO分解的多种机制的结果。内皮细胞中氧化还原平衡的改变导致超氧阴离子产生增加和氧化应激。这反过来不仅对血管张力产生负面影响,而且还能够激活重要的机制(如血小板活性、白细胞粘附、血管平滑肌细胞增殖和粘附分子的表达),在高血压靶器官损伤的发病机制中具有确定的中心作用。因此,与降低血压本身相比,能够恢复原发性高血压患者NO可用性的药物治疗可能会在预防靶器官损伤和改善这些患者的预后方面发挥额外的益处。不幸的是,到目前为止,只有肾素-血管紧张素系统的拮抗剂和钙通道阻滞剂在这方面表现出一定的能力,而没有纵向干预研究已经进行,到目前为止,证明NO生物利用度的恢复,通过抗高血压治疗可能会赋予额外的预后优势,原发性高血压患者。
A major cause for endothelial dysfunction in essential hypertension is decreased availability of nitric oxide (NO). Impairment in NO bioavailability is likely to be the consequence of multiple mechanisms affecting NO synthesis as well as NO breakdown. An alteration in the redox balance in endothelial cells leads to increased superoxide anion production and oxidative stress. This in turn not only exerts negative effects on vascular tone, but is also able to activate important mechanisms (such as platelet activity, leukocyte adhesion, vascular smooth muscle cell proliferation and expression of adhesion molecules) with an established central role in the pathogenesis of hypertensive target organ damage. As a consequence, a drug therapy able to restore NO availability in essential hypertensive patients would probably exert additional benefits, as compared to blood pressure lowering per se, in terms of prevention of target organ damage and improved prognosis of these patients. Unfortunately, as of today only the antagonists of the renin-angiotensin system and the calcium-channel blockers have shown some ability in this respect, whereas no longitudinal intervention study has been undertaken, so far, to prove that the restoration of NO bioavailability through an antihypertensive treatment may confer additional prognostic advantage to essential hypertensive patients.