Bragulat E, de la Sierra A, Antonio M T, Coca A
Hypertension Unit, Department of Internal Medicine, Institut d'Investigacions Biomèdiques August Pi i Sunyer, Hospital Clínic, Barcelona, Spain.
Hypertension. 2001 Feb;37(2 Pt 2):444-8. doi: 10.1161/01.hyp.37.2.444.
The aim of this study was to evaluate endothelium-dependent and -independent vasodilation, as well as endothelium biochemical markers, in a group of essential hypertensive patients classified on the basis of salt sensitivity. Changes in forearm blood flow in response to acetylcholine, sodium nitroprusside, and N(G)-monomethyl-L-arginine (L-NMMA) infusion were determined by means of strain-gauge plethysmography. Moreover, plasma and urinary concentrations of nitrates, cGMP, and endothelin were measured during low (50 mmol/d) and high (250 mmol/d) salt intake. Salt-sensitive hypertension was diagnosed in 26 patients who exhibited a significant increase in 24-hour mean blood pressure assessed by ambulatory blood pressure monitoring after 1 week of high salt intake. Nineteen patients were considered salt resistant. Compared with salt-resistant hypertensives, salt-sensitive patients presented a significant lower (P=0.005) maximal acetylcholine-induced vasodilation (21+/-6.3 versus 28+/-7.5 mL. 100 mL(-1). tissue. min(-1)). On the contrary, maximal sodium nitroprusside-induced vasodilation did not significantly differ between groups (22.4+/-4.5 versus 23.9+/-5.3 mL. 100 mL(-1). tissue. min(-1)). The decrease in maximal acetylcholine-induced vasodilation promoted by the coadministration of L-NMMA was significantly more pronounced in salt-resistant compared with salt-sensitive patients (P=0.003). Finally, high salt intake promoted a significant decrease in 24-hour urinary nitrate excretion in salt-sensitive patients (from 443+/-54 to 312+/-54 micromol/d; P=0.033) compared with salt-resistant hypertensives (from 341+/-50 to 378+/-54 micromol/d). We conclude that salt-sensitive hypertension is associated with endothelial dysfunction characterized by a defective endothelium-dependent vasodilation. Impairment of the L-arginine-nitric oxide pathway may be responsible for this abnormal endothelial response.
本研究的目的是评估一组根据盐敏感性分类的原发性高血压患者的内皮依赖性和非内皮依赖性血管舒张以及内皮生化标志物。通过应变片体积描记法测定乙酰胆碱、硝普钠和N(G)-单甲基-L-精氨酸（L-NMMA）输注后前臂血流量的变化。此外，在低盐（50 mmol/d）和高盐（250 mmol/d）摄入期间测量血浆和尿液中的硝酸盐、环磷酸鸟苷（cGMP）和内皮素浓度。通过动态血压监测，在高盐摄入1周后，26例24小时平均血压显著升高的患者被诊断为盐敏感性高血压。19例患者被认为是盐抵抗性的。与盐抵抗性高血压患者相比，盐敏感性患者乙酰胆碱诱导的最大血管舒张显著降低（P=0.005）（分别为21±6.3与28±7.5 mL·100 mL⁻¹·组织·min⁻¹）。相反，两组之间硝普钠诱导的最大血管舒张无显著差异（分别为22.4±4.5与23.9±5.3 mL·100 mL⁻¹·组织·min⁻¹）。与盐敏感性患者相比，联合使用L-NMMA时，盐抵抗性患者乙酰胆碱诱导的最大血管舒张降低更为显著（P=0.003）。最后，与盐抵抗性高血压患者（从341±50降至378±54 μmol/d）相比，高盐摄入使盐敏感性患者24小时尿硝酸盐排泄显著降低（从443±54降至312±54 μmol/d；P=0.033）。我们得出结论，盐敏感性高血压与以内皮依赖性血管舒张缺陷为特征的内皮功能障碍有关。L-精氨酸-一氧化氮途径的受损可能是这种异常内皮反应的原因。
