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高血压中的L-精氨酸-一氧化氮途径

The L-arginine-nitric oxide pathway in hypertension.

作者信息

Kelm Malte

机构信息

Medizinische Klinik und Poliklinik B, Klinik für Kardiologie, Pneumologie und Angiologie, Moorenstrasse 5, 40225 Düsseldorf, Germany.

出版信息

Curr Hypertens Rep. 2003 Feb;5(1):80-6. doi: 10.1007/s11906-003-0015-z.

DOI:10.1007/s11906-003-0015-z
PMID:12530940
Abstract

Nitric oxide is involved in the regulation of resting vascular tone, adaptation of blood flow to metabolic demand of tissue, and adaptation of vessel diameter to volume of inflow, ie, flow-mediated dilation. Arterial hypertension is associated with an increased vascular tone of resistance vessels, a reduced compliance of conduit arteries, along with a thickening of the intima-media leading to vascular remodeling. Dysfunctional endothelium triggers such maladaptive processes. A reduced bioavailability of nitric oxide has been shown in hypertensive individuals dependent on the duration and severity of arterial hypertension. Angiotensin-converting enzyme inhibitors reverse endothelial dysfunction, whereas a concomitant reduction in significant cardiac events due to improved bioavailability has yet to be established. Long-term follow-up studies in individuals with manifest endothelial dysfunction and in offspring from hypertensive patients underscore the prognostic and genetic significance of a reduced nitric oxide bioavailability for the pathophysiology of arterial hypertension.

摘要

一氧化氮参与静息血管张力的调节、血流对组织代谢需求的适应以及血管直径对流入量的适应,即血流介导的血管舒张。动脉高血压与阻力血管的血管张力增加、传导动脉顺应性降低以及内膜中层增厚导致血管重塑有关。功能失调的内皮会引发这种适应不良的过程。一氧化氮生物利用度降低在高血压个体中已得到证实,且取决于动脉高血压的持续时间和严重程度。血管紧张素转换酶抑制剂可逆转内皮功能障碍,然而,由于生物利用度改善而导致重大心脏事件显著减少这一点尚未得到证实。对有明显内皮功能障碍的个体以及高血压患者后代进行的长期随访研究强调了一氧化氮生物利用度降低在动脉高血压病理生理学中的预后和遗传意义。

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