Abstract

Background: Several reports have shown that circulating, soluble cellular adhesion molecules and endothelin-1 (ET-1) are implicated in the pathophysiological events of atherosclerosis and may reflect the endothelial dysfunction characterizing this disorder. Methods: To evaluate the expression of these factors in arterial hypertension (AH), we measured plasma levels of soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble P-selectin (sP-selectin), and ET-1 in 60 untreated patients with mild to moderate AH (hypercholesterolemic: n=31, normocholesterolemic: n=29) and 30 sex- and age-matched normocholesterolemic normotensive controls. Results: Hypertensive patients exhibited significantly higher levels of sICAM-1 (234±21 vs. 187±12 ng/ml, P<0.005), sVCAM-1 (681±42 vs. 589±23 ng/ml, P<0.005), sP-selectin (89±17 vs. 55±11 ng/ml, P<0.01) and ET-1 (6.2±0.7 vs. 2.4±0.3 pg/ml, P<0.01) than did normotensive controls. The normocholesterolemic hypertensives had lower levels of sICAM-1, sVCAM-1 ( P<0.01), sP-selectin and ET-1 ( P<0.05) than hypercholesterolemic hypertensives, but higher levels than normotensive controls ( P<0.05). In hypertensives, plasma ET-1 was significantly correlated with mean arterial pressure ( r=0.51, P<0.03) and sICAM-1 levels ( r=0.64, P<0.01). In hypercholesterolemic hypertensives, LDL cholesterol was also significantly correlated with plasma levels of sICAM-1 ( r=0.53, P<0.04) and sP-selectin ( r=0.41, P<0.05). Conclusions: Plasma levels of soluble cellular adhesion molecules are elevated in hypertensive patients in comparison to normotensive controls and may be related to plasma ET-1 activity. The coexistence of hypercholesterolemia may enhance the plasma soluble adhesion molecule activity induced by AH.

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