engleski

The dynamics of cell adhesion molecules and their ligands expression in hypertensive patients on Ca-channel blocker therapy

Objective: To determine the effect of arterial blood pressure (BP) reduction on soluble cell adhesion molecules' (sCAM) and endocan plasma concentration and the expression of their ligands on circulatory leukocyte subpopulations. Design and Methods: 20 newly discovered hypertensive subjects of both sexes (age: 53±8 yrs) were treated with Ca-channel blocker, amlodipin (5-10mg/day for 8 weeks ; dose to reach BP≤139/89 mmHg). The serum sCAMs and endocan concentrations were determined by commercially available ELISA kits. Level of sCAMs ligands on lymphocytes, monocytes and granulocytes was assessed by flow cytometry. Paired t-test, or t-test were used as appropriate, with Pearson’s correlation calculated ; results are presented as mean±SD (SigmaPlot v.11). Results: Serum levels of sICAM-1 and sVCAM-1 were significantly decreased (p≤0.001 and p=0.002, respectively), while E-selectin levels were significantly increased after the amlodipin treatment (P=0.014). Endocan levels tended to decrease with BP reduction (p=0.063). Expression of CD11a/LFA-1 (ICAM-1 and endocan ligand) was significantly increased in all three cell types with BP decrease (Ly p=0.009, Mo p≤0.001, Gr p=0.005). CD15 (E-selectin ligand) showed weak reactivity on lymphocytes and monocytes, but it was abundant on granulocytes. CD15 and CD49d/VLA-4 (VCAM-1 ligand) did not change significantly after the treatment. All three ligands showed significantly different pattern of expression on various cell types (p≤0.001). There was significant positive correlation of systolic and diastolic BP with ICAM-1 and VCAM-1, and negative correlation of systolic BP with their respective leukocyte ligands, reaching significance for granulocyte and monocyte CD11a/LFA-1. Endocan significantly positively correlated with ICAM-1. Conclusions: The increased expression of sCAMs’ ligands on circulatory leukocytes, together with significant decrease of endothelial CAMs and endocan after amlodipin treatment suggests the de-activation of the endothelium with successful reduction in blood pressure. This potentially decreases the adherence of circulatory leukocytes to endothelium possibly via endocan regulated pathway and subsequently decreases the risk for development of atherosclerotic lesions.

solubile cellular adhesion molecules; CD11a/LFA-1; CD15; hypertension

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