Integrative Vascular Biology Laboratory, Department of Integrative Physiology, University of Colorado, Boulder, Colorado, USA.
Am J Hypertens. 2011 Sep;24(9):976-81. doi: 10.1038/ajh.2011.88. Epub 2011 Jun 2.
Endothelial vasodilator dysfunction contributes to the development of hypertension (blood pressure (BP) ≥ 140/90 mm Hg) and cardiovascular disease (CVD). Prehypertension (BP 120-139/80-89 mm Hg) has recently been identified as an independent risk factor for hypertension and CVD. It is currently unclear whether BP in the prehypertensive range is associated with endothelial vasodilator dysfunction. We tested the hypothesis that BP in the prehypertensive range, independent of other cardiovascular risk factors, is associated with impaired nitric oxide (NO)-mediated endothelium-dependent vasodilation.
Forearm blood flow (FBF) responses to intra-arterial acetylcholine (ACh; 8.0-32.0 µg/100 ml tissue/min) and sodium nitroprusside (SNP; 1.0-4.0 µg/100 ml tissue/min) were measured in 20 normotensive (age: 56 ± 1 years; BP: 110/70 ± 1/2 mm Hg) and 20 prehypertensive (56 ± 2 years; 128/79 ± 2/2 mm Hg) adults. In addition, FBF responses to ACh were determined in the absence and presence of the endothelial NO synthase inhibitor N(G)-monomethyl-L-arginine (L-NMMA) (5 mg/min).
FBF responses to ACh were significantly lower (30%) in prehypertensive (from 4.2 ± 0.3 to 11.4 ± 0.7 ml/100 ml tissue/min) compared with normotensive (from 4.6 ± 0.2 to 14.5 ± 0.7 ml/100 ml tissue/min) adults. There were no group differences in FBF responses to SNP. Co-infusion of L-NMMA significantly reduced the FBF response to ACh in the normotensive (30%; P <0.05) but not the prehypertensive adults.
Prehypertension is associated with impaired NO-mediated endothelium-dependent vasodilation. The endothelial vasodilator dysfunction that characterizes hypertension is present at BP levels in the prehypertensive range and may contribute to the increased risk of hypertension and CVD in this population.
内皮血管舒张功能障碍是高血压（血压≥140/90mmHg）和心血管疾病（CVD）发展的原因之一。最近发现，高血压前期（血压 120-139/80-89mmHg）是高血压和 CVD 的独立危险因素。目前尚不清楚高血压前期范围内的血压是否与内皮血管舒张功能障碍有关。我们检验了以下假设，即在不考虑其他心血管危险因素的情况下，高血压前期范围内的血压与一氧化氮（NO）介导的内皮依赖性血管舒张功能受损有关。
通过测量肱动脉血流（FBF）对乙酰胆碱（ACh；8.0-32.0μg/100ml 组织/分钟）和硝普钠（SNP；1.0-4.0μg/100ml 组织/分钟）的反应，来评估 20 名血压正常（年龄：56±1 岁；血压：110/70±1/2mmHg）和 20 名高血压前期（56±2 岁；128/79±2/2mmHg）成年人的内皮功能。此外，在存在和不存在内皮型一氧化氮合酶抑制剂 N(G)-单甲基-L-精氨酸（L-NMMA）（5mg/min）的情况下，还测定了 ACh 引起的 FBF 反应。
与血压正常（从 4.6±0.2 增加到 14.5±0.7ml/100ml 组织/分钟）的成年人相比，高血压前期（从 4.2±0.3 增加到 11.4±0.7ml/100ml 组织/分钟）的 ACh 引起的 FBF 反应明显降低（约 30%）。对 SNP 的 FBF 反应在两组之间没有差异。在正常血压成年人中，同时输注 L-NMMA 显著降低了 ACh 引起的 FBF 反应（约 30%；P<0.05），但在高血压前期成年人中没有。
高血压前期与一氧化氮介导的内皮依赖性血管舒张功能障碍有关。高血压特征性的内皮血管舒张功能障碍存在于高血压前期范围内的血压水平，可能导致该人群高血压和 CVD 的风险增加。
