IMPAIRED ENDOTHELIUM-DEPENDENT VASODILATION IN PATIENTS WITH ESSENTIAL-HYPERTENSION - EVIDENCE THAT NITRIC-OXIDE ABNORMALITY IS NOT LOCALIZED TO A SINGLE SIGNAL-TRANSDUCTION PATHWAY
IMPAIRED ENDOTHELIUM-DEPENDENT VASODILATION IN PATIENTS WITH ESSENTIAL-HYPERTENSION - EVIDENCE THAT NITRIC-OXIDE ABNORMALITY IS NOT LOCALIZED TO A SINGLE SIGNAL-TRANSDUCTION PATHWAY
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DOI：
10.1161/01.cir.91.6.1732
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发表时间：
1995-03-15
期刊：
影响因子：
37.8
通讯作者：
CANNON, RO
中科院分区：
文献类型：
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作者：
PANZA, JA;GARCIA, CE;CANNON, RO
背景：原发性高血压患者存在内皮依赖性血管松弛异常，这在很大程度上与一氧化氮（NO）生物活性降低有关。本研究的目的是确定这种缺陷是由于特定细胞内信号转导途径水平的缺陷还是更广泛的内皮异常的结果。方法与结果研究了10例高血压患者（男5例，女5例，年龄48+/-9岁[mean+/-SD]）和12例对照组（男6例，女6例，年龄48+/-7岁）前臂血管对乙酰胆碱和缓激肽（通过不同信号转导途径起作用的内皮依赖性药物）和硝普钠（血管平滑肌直接扩张剂）的反应。为了确定NO对缓激肽诱导的血管舒张的作用，在给予n- g -单甲基- l-精氨酸（一种抑制NO合成的精氨酸类似物）后，还测量了血管对缓激肽的反应。将药物注入肱动脉，用应变计体积描记仪测量前臂血流量。高血压患者对乙酰胆碱的反应明显减弱（最大血流量为7.5+/-2 mL对16.6+/-8 mL）。分钟(1)。对照组100 mL(-1)[平均+/-SD]；P
Background Patients with essential hypertension have abnormal endothelium-dependent vascular relaxation, largely related to reduced bioactivity of nitric oxide (NO). The purpose of the present investigation was to determine whether this defect is due to a deficit at the specific intracellular signal-transduction pathway level or is a consequence of a more generalized endothelial abnormality.Methods and Results The responses of the forearm vasculature to acetylcholine and bradykinin (endothelium-dependent agents that act through different signal transduction pathways) and to sodium nitroprusside (a direct dilator of vascular smooth muscle) were studied in 10 hypertensive patients (5 men, 5 women; aged 48+/-9 years old [mean+/-SD]) and 12 control subjects (6 men, 6 women; aged 48+/-7 years old). To determine the contribution of NO to bradykinin-induced vasodilation, the vascular responses to bradykinin were also measured after administration of N-G-monomethyl-L-arginine, an arginine analogue that inhibits the synthesis of NO. Drugs were infused into the brachial artery, and forearm blood flow was measured by strain-gauge plethysmography. The response to acetylcholine was significantly blunted in hypertensive patients (maximal blood flow, 7.5+/-2 versus 16.6+/-8 mL . min(-1). 100 mL(-1) in control subjects [mean+/-SD]; P