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POTENTIATION OF ENDOTHELIUM-DEPENDENT VASODILATION IN HUMANS BY L-ARGININE

POTENTIATION OF ENDOTHELIUM-DEPENDENT VASODILATION IN HUMANS BY L-ARGININE
L-精氨酸增强人体内皮依赖性血管舒张作用
批准号:
3843417
负责人:
J A PANZA
金额:
$0.0万
依托单位国家:
美国
项目类别:
财政年份:
--
资助国家:
美国
项目状态:
未结题
起止时间:
至

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中文摘要
翻译
L精氨酸是内皮源性一氧化氮的天然前体, 内皮细胞调节血管张力的中介物。这个 目前的调查是为了确定是否增加了 内皮细胞中一氧化氮前体的可用性可以 增强对内皮依赖性血管扩张剂的反应。为了这个 目的:正常受试者12例,年龄49±7岁,男7例,女5例。 输注血管内皮细胞依赖的乙酰胆碱进行研究 血管扩张剂和硝普钠,一种直接的平滑肌扩张剂, 输注L-精氨酸前后比较。D-精氨酸的作用 不是一氧化氮前体的异构体)对 对其中8名受试者进行了乙酰胆碱研究。毒品被注入到 对前臂动脉血流的反应是 用应变计体积描记法测量。在注入的剂量下(40 微米/分),L-精氨酸或D-精氨酸不改变血流。然而, 用L-精氨酸观察乙酰胆碱对血管扩张的反应 显著大于单独使用乙酰胆碱的情况。 反之,L-精氨酸不能改变钠的反应 硝普钠。此外,D-不改变对乙酰胆碱的反应。 精氨酸。这些发现表明了前驱体的可用性 内皮衍生的一氧化氮是内皮细胞的限速步骤- 人类依赖的血管松弛。
英文摘要
L-arginine is the natural precursor of endothelium-derived nitric oxide, a mediator in the regulation of vascular tone by endothelial cells. The present investigation was undertaken to determine whether increased availability of nitric oxide precursor in the endothelial cells can potentiate the response to endothelium-dependent vasodilators. For this purpose, 12 normal subjects (age 49+7 years; 7 males and 5 females) were studied with infusion of acetylcholine, an endothelium-dependent vasodilator and sodium nitroprusside, a direct smooth muscle dilator, before and after the infusion of L-arginine. The effect of D-arginine (an isomer that is not a precursor of nitric oxide) on the response to acetylcholine was studied in 8 of these subjects. Drugs were infused into the brachial artery and the response of the forearm blood flow was measured by strain gauge plethysmography. At the doses infused (40 microm/min), L-arginine or D-arginine did not change blood flow. However, the vasodilator response to acetylcholine observed with L-arginine was significantly greater than that observed with acetylcholine alone. Conversely, L-arginine did not modify the response to sodium nitroprusside. Also, the response to acetylcholine was not modified by D- arginine. These findings indicate the availability of precursor of endothelium-derived nitric oxide is a rate-limiting step in endothelium- dependent vascular relaxation in humans.
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