This study shows a homogeneous coefficient of variation for FMD among different centers. The inter-session coefficient of variation was similar to the intra-session coefficient of variation, representing the intrinsic FMD variability. We demonstrate for the first time that rigorous and standardized procedure may provide reproducible FMD assessment to study endothelial function in multicenter clinical trials.

Abstract-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 (nϭ18) or salt resistant (nϭ21) according to their blood pressure responses to changes in dietary NaCl intake. Salt-sensitive hypertensives showed higher plasma ET-1 (PϽ0.05), vWf (PϽ0.005), and S-E-selectin levels (PϽ0.04) and increased UAE (PϽ0.05) than salt-resistant hypertensives. By contrast, circulating S-ICAM-1 and S-VCAM-1 concentrations were not significantly higher in salt-sensitive (596.56Ϯ177.05 ng/mL and 541.06Ϯ157.84 ng/mL, respectively) than salt-resistant patients (516.86Ϯ147.99 ng/mL and 449.48Ϯ158.91 ng/mL, respectively). During the intermediate NaCl diet, plasma ET-1 responses to oral glucose load were greater in salt-sensitive (PϽ0.05) than in salt-resistant patients. A marked (PϽ0.05) 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. (Hypertension. 1998;32:862-868.)Key Words: endothelium Ⅲ cell adhesion molecules Ⅲ vasorelaxation Ⅲ sodium Ⅲ blood pressure S alt-sensitive hypertension is characterized by a cluster of renal, hormonal, and metabolic derangements that might favor the development of cardiovascular and renal complications.1,2 In this regard, the vascular endothelium modulates platelet aggregation, adhesion molecule expression, and vascular smooth muscle cell replication, 3 all of which contribute to atherogenesis. Interestingly, salt-sensitive hypertension is characterized by impaired endothelium-dependent vasorelaxation. 4 Furthermore, circulating levels of the endotheliumderived peptide endothelin-1 (ET-1) are higher, 5 while urinary ET-1 excretion is lower 6 and more responsive to salt loading 7 in salt-sensitive than salt-resistant patients. Urinary albumin excretion (UAE), a well-known marker of vascular damage, 8 is associated with high plasma levels of von Willebrand factor (vWf,) 9 a glycoprotein released by damaged vascular endotheli...

Aims-To evaluate the behaviour ofplasma endothelin-1 in patients with chronic hypoxia. Methods-Fifteen male patients (mean age 52-1 + 3-1 years) with mild chronic obstructive pulmonary disease (COPD) were studied. Twelve healthy men (mean age 48 3 +5 54 years) served as controls. Both patients and controls underwent standard pulmonary function tests, echocardiographic evaluation, and arterial blood gas evaluation. Blood samples for endothelin-l assay were taken from a previously incannulated antecubital vein after 60 minutes of rest in the supine position.

This is the first large and systematic analysis of the relationship between detailed ECG abnormalities and MAU/chronic kidney disease in hypertensive patients without overt cardiovascular diseases. We report a significant and independent relationship between the presence of ECG abnormalities and renal damage in a preclinical stage of hypertension. Identification of ECG abnormalities in hypertension should prompt physicians to careful detection for renal damage, also in order to achieve an accurate risk stratification.

1. The behaviour of the potent vasoconstrictive endothelium-derived peptide endothelin-1 was evaluated in salt-sensitive hypertension. 2. Circulating and urinary endothelin-1 levels were evaluated in 30 men (mean age 44.6 +/- 3.1 years) with uncomplicated essential hypertension after three consecutive 2-week periods on an intermediate (120 mmol), low (20 mmol) and high (240 mmol) NaCl diet. On the same occasions, blood pressure was measured to identify salt-sensitive patients (n = 16), i.e. those patients showing a mean blood pressure increase > 10 mmHg when switching from a low to a high NaCl diet, and salt-resistant patients (n = 14), i.e. those who did not show such mean blood-pressure variations. 3. Plasma endothelin-1 levels were higher (P < 0.005) in salt-sensitive than in salt-resistant hypertensive patients after intermediate-, low- and high-NaCl diets. Urinary endothelin-1 excretion was similar in both groups after an intermediate-NaCl diet, whereas it was significantly higher in salt-sensitive than in salt-resistant hypertensive subjects after low (P < 0.002) and high (P < 0.007) NaCl diets. High NaCl intake induced a significant increase in plasma endothelin-1 levels (P < 0.002) as compared with intermediate and low NaCl diet levels in salt-sensitive patients, but did not in salt-resistant subjects. No significant NaCl intake-related variations of urinary endothelin-1 excretion were observed in either group. 4. Salt-sensitive hypertensives are characterized by increased levels of endothelin-1 in both plasma and urine. This fact suggests that blood-pressure sensitivity to NaCl intake could be associated with an increased risk of developing both renal and cardiovascular damage.