Effects of severe, uncontrolled hypertension on endothelial activation: soluble vascular cell adhesion molecule-1,...

The molecular mechanisms whereby severe, uncontrolled hypertension (SHT) is translated into acute vascular target organ dysfunction have not been completely defined. We sought to determine whether SHT is associated with pressure-dependent endothelial activation as assessed by soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble intercellular adhesion molecule-1 (sICAM-1) and von Willebrand Factor (vWF).

We determined sVCAM-1, sICAM-1 and vWF in three groups: (i) untreated patients referred specifically for treatment of SHT [diastolic blood pressure (DBP) > or = 120 mm Hg; n = 24]; (ii) untreated patients with established mild hypertension (MHT; DBP 95-100 mmHg; n = 19); and (iii) normotensive volunteers (DBP < or = 90; n = 16).

By analysis of variance, sVCAM-1 (P = 0.002), sICAM-1 (P = 0.02) and vWF (P = 0.009) were greater in SHT and MHT than in normotensives but did not differ between SHT and MHT. We observed a significant positive correlation between blood pressure and soluble activation markers at lower blood pressures (normotensives and MHT considered together) that was not present in SHT.

Even mild elevation of blood pressure may be sufficient to activate the expression of adhesion molecules. Mechanisms other than the endothelial expression of adhesion molecules may be important in mediating the accelerated target organ injury produced by SHT in humans. Concentrations of soluble adhesion molecules and vWF may depend more strongly upon factors in the hypertensive microenvironment other than the absolute level of blood pressure.