The role of nitric oxide in hypertension and renal disease progression
The role of nitric oxide in hypertension and renal disease progression
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DOI：
10.1093/ndt/16.suppl_1.60
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发表时间：
2001-01-01
影响因子：
6.1
通讯作者：
Klahr, S
中科院分区：
文献类型：
--
作者：
Klahr, S
内皮型一氧化氮合酶（eNOS）在血管系统中发挥多种功能。在响应刺激，如剪切应力或乙酰胆碱，eNOS催化-从L-精氨酸的一氧化氮（NO）的生产。NO扩散穿过内皮进入邻近的平滑肌并诱导血管舒张。NO还在局部起作用以防止血小板和白细胞聚集并抑制血管平滑肌细胞增殖。已经表明，缺乏eNOS的小鼠具有降低的血压、降低的心率和增加的血浆肾素活性。也有报道称，与血压正常的个体相比，原发性高血压患者的NO产生减少。在几种肾脏疾病的动物模型（次全肾消融术，输尿管梗阻和糖尿病），L-精氨酸的管理，并可能增加NO的合成，降低肾小球硬化的程度，改善了肾小管间质室的肾脏的变化，也减少了浸润的巨噬细胞的肾脏。总之，L-精氨酸-NO通路在高血压、肾脏疾病、炎症和动脉粥样硬化中起重要作用。该途径还与肾素-血管紧张素系统、类花生酸途径、内皮素、细胞因子和炎症调节因子如NF-κ B相互作用。
Endothelial nitric oxide synthase (eNOS) serves a number of functions in the vasculature. In response to stimuli such as shear stress or acetylcholine, eNOS catalyses-the production of nitric oxide (NO) from L-arginine. The NO diffuses across the endothelium into neighbouring smooth muscle and induces vasodilation. NO also acts locally to prevent platelet and leucocyte aggregation and inhibits vascular smooth muscle cell proliferation. It has been shown that mice lacking eNOS have decreased blood pressure, decreased heart rate and increased plasma renin activity. It has also-been reported that NO production was reduced in patients with essential hypertension compared with normotensive individuals. In several animal models of renal disease (subtotal renal ablation, ureteral obstruction and diabetes), the administration of L-arginine, and probably the increase in NO synthesis, reduced the degree of glomerulosclerosis, ameliorated the changes in the tubulointerstitial compartment of the kidney and also decreased the infiltration of the kidney by invading macrophages. In summary, the L-arginine-NO pathway plays an important role in hypertension, renal disease, inflammation and atherosclerosis. This pathway also interacts with the renin-angiotensin system, the eicosanoid pathway, endothelin, cytokines and regulators of inflammation such as NF-kappaB.