he vascular endothelial surface has an intrinsic capacity to prevent cardiovascular disease through modulation of arterial tone, thrombosis, inflammation and structural changes by releasing vasoactive agents, in particular, nitric oxide (NO). [1][2][3] Endothelial cells in hypertensive disease are the target of blood pressure increases, which impair endothelial function and precede cardiovascular structural changes such as vascular and myocardial remodeling and hypertrophy. [4][5][6] Abnormal endotheliumdependent vascular relaxation in patients with primary hypertension has been described 7 and is associated with abnormalities of the NO system. 8,9 Low-renin (volume-dependent 10 hypertension (VDH)) is an important subset of primary hypertension (25-30% of patients), and is characterized by specific biological and pathophysiological clinical features such as salt-sensitivity and increased diuretic response, as well as heterogeneous blood pressure increments in response to high dietary salt intake. [11][12][13] Animal studies have demonstrated that reduced NO production favors the development of salt-sensitive hypertension. 14 Studies in salt-sensitive hypertensive patients have reported defective endothelium-dependent vasodilation in the forearm assessed using strain-gauge plethysmography, suggesting that abnormalities of the NO system are implicated in the development of salt-sensitive hypertension. [15][16][17] However, the association between the low-renin state and endothelial dysfunction has not been adequately investigated and the pathophysiological mechanisms involved remain unclear. Carotid arterial wall thickness assessed by intima-media thickness (IMT) has been shown to have an association with cardiovascular risk factors of atherosclerosis such as hypertension, hypercholesterolemia, diabetes and smoking. [18][19][20] Recent evidence has shown that an increased carotid IMT is a strong predictor of coronary heart disease and strokes. 21 Vascular reactivity evaluated by flow-mediated dilation (FMD) 22,23 and the vascular remodeling reflected by carotid IMT measurements are adequately assessed by highresolution ultrasound examinations. 19 The aim of this study was to evaluate the FMD in the brachial artery and vascular remodeling of the distal common carotid artery by measuring the IMT using highresolution ultrasound in hypertensive subjects subdivided according to plasma renin activity (PRA) as either volume dependent (VDH; low-renin, PRA <0.6 ng· ml -1 · h -1 ) or renin dependent (RDH; PRA >0.6 ng·ml -1 ·h -1 ) after balanced urinary sodium excretion. 11,12 (VDH) is not yet known. To evaluate this, flow-mediated dilation (FMD) of the brachial artery and the carotid intima-media thickness in the distal common carotid artery were measured and compared between renin-dependent mild-hypertensive patients (RDH) and controls. Method and ResultsThe study group comprised 40 mild-hypertensive patients and 25 controls. Plasma renin activity (PRA), plasma aldosterone concentration, angiotensin II and nitrite/nitrate...

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