Ferri C, Bellini C, Desideri G, Giuliani E, De Siati L, Cicogna S, Santucci A
University "La Sapienza," Chair of I Clinica Medica, Andrea Cesalpino Foundation, Departments of Experimental Medicine, A.S.), University of L'Aquila, L'Aquila, Italy.
Hypertension. 1998 Nov;32(5):862-8. doi: 10.1161/01.hyp.32.5.862.
The contributing role of vascular endothelium in the development of hypertension-related vascular damage is well accepted. Salt-sensitive hypertension is characterized by a cluster of renal, hormonal, and metabolic derangements that might favor the development of cardiovascular and renal damage. To evaluate endothelial involvement in salt-sensitive essential hypertension, plasma levels of several markers of endothelial damage such as endothelin-1 (ET-1), von Willebrand factor (vWf), and soluble (S-) adhesion molecules E-selectin, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and 24-hour urinary albumin excretion (UAE) were measured in 39 nondiabetic, nonobese, never-treated essential hypertensive patients after intermediate (120 mmol/d), high (220 mmol/d), and low (20 mmol/d) NaCl diets. Patients were classified as salt sensitive (n=18) or salt resistant (n=21) according to their blood pressure responses to changes in dietary NaCl intake. Salt-sensitive hypertensives showed higher plasma ET-1 (P<0.05), vWf (P<0.005), and S-E-selectin levels (P<0.04) and increased UAE (P<0.05) than salt-resistant hypertensives. By contrast, circulating S-ICAM-1 and S-VCAM-1 concentrations were not significantly higher in salt-sensitive (596. 56+/-177.05 ng/mL and 541.06+/-157.84 ng/mL, respectively) than salt-resistant patients (516.86+/-147.99 ng/mL and 449.48+/-158.91 ng/mL, respectively). During the intermediate NaCl diet, plasma ET-1 responses to oral glucose load were greater in salt-sensitive (P<0. 05) than in salt-resistant patients. A marked (P<0.05) hyperinsulinemic response to oral glucose load was evident in salt-sensitive but not salt-resistant patients after each diet. This study shows increased plasma levels of the endothelium-derived substances E-selectin, vWf, and ET-1 in salt-sensitive hypertensives. Our findings support the hypothesis that salt sensitivity is correlated with an increased risk for developing hypertension-related cardiovascular damage.
血管内皮在高血压相关血管损伤发展过程中的作用已得到广泛认可。盐敏感性高血压的特征是一系列肾脏、激素和代谢紊乱，这些紊乱可能促进心血管和肾脏损伤的发展。为了评估内皮细胞在盐敏感性原发性高血压中的作用，我们对39例非糖尿病、非肥胖、未经治疗的原发性高血压患者在摄入中等量（120 mmol/d）、高量（220 mmol/d）和低量（20 mmol/d）氯化钠饮食后，检测了几种内皮损伤标志物的血浆水平，如内皮素-1（ET-1）、血管性血友病因子（vWf）以及可溶性（S-）黏附分子E-选择素、细胞间黏附分子-1（ICAM-1）、血管细胞黏附分子-1（VCAM-1），并测定了24小时尿白蛋白排泄量（UAE）。根据患者对饮食中氯化钠摄入量变化的血压反应，将患者分为盐敏感型（n = 18）和盐抵抗型（n = 21）。盐敏感型高血压患者的血浆ET-1（P < 0.05）、vWf（P < 0.005）和S-E-选择素水平（P < 0.04）更高，UAE也增加（P < 0.05），高于盐抵抗型高血压患者。相比之下，盐敏感型患者（分别为596.56 ± 177.05 ng/mL和541.06 ± 157.84 ng/mL）循环中的S-ICAM-1和S-VCAM-1浓度并不显著高于盐抵抗型患者（分别为516.86 ± 147.99 ng/mL和449.48 ± 158.91 ng/mL）。在中等量氯化钠饮食期间，盐敏感型患者口服葡萄糖负荷后血浆ET-1反应大于盐抵抗型患者（P < 0.05）。在每种饮食后，盐敏感型患者对口服葡萄糖负荷有明显的高胰岛素血症反应（P < 0.05），而盐抵抗型患者则无。本研究表明，盐敏感型高血压患者血浆中内皮源性物质E-选择素、vWf和ET-1水平升高。我们的研究结果支持了盐敏感性与高血压相关心血管损伤发生风险增加相关的假说。
