title: The effects of arterial blood pressure reduction on endocan and soluble endothelial cell adhesion molecules (CAMs) and CAMs ligands expression in hypertensive patients on Ca-channel blocker therapy.
abstract: OBJECTIVE
  To determine the effect of arterial blood pressure (BP) reduction on endocan and soluble cell adhesion molecules' (sCAM) plasma concentration and expression of their ligands on circulatory leukocyte subpopulations.
  
  
  METHODS
  24 hypertensive subjects of both sexes (age: 53±8 yrs) were treated with Ca-channel blocker, amlodipin (5-10 mg/day for 8 weeks; to reach BP≤139/89mmHg). The serum sCAMs and endocan concentrations were determined by ELISA kits. Level of ICAM/VCAM ligands on leukocytes was assessed by flow cytometry. Paired t-test, or t-test were used as appropriate, with Pearson's correlation calculated; p<0.05 was considered significant (SigmaPlot v.11).
  
  
  RESULTS
  sICAM-1 and sVCAM-1 were decreased (p≤0.001 and p=0.002, respectively), while E-selectin concentration was increased after amlodipin treatment (P=0.014). CD11a/LFA-1 (ICAM-1 and endocan ligand) was significantly increased in all three cell types with BP decrease. CD15 and CD49d/VLA-4 (VCAM-1 ligand) did not change after the treatment. There was significant positive correlation of systolic and diastolic BP with ICAM-1 and VCAM-1, and significant negative correlation of systolic BP with CD11a/LFA-1. Endocan significantly positively correlated with ICAM-1.
  
  
  CONCLUSIONS
  The increased expression of ICAM/VACM ligands, together with decrease of sCAMs and endocan suggests the de-activation of endothelium with reduction in BP, decreasing the adherence of circulatory leukocytes to endothelium; subsequently decreasing the risk for development of atherosclerosis.
authors.affiliation: Gesundheitszentrum Lange Reihe Dr. Tadzic und Kollegen, Hamburg, Germany.
authors.forename: Refmir
authors.initials: R
authors.lastname: Tadzic
authors.forename: Martina
authors.initials: M
authors.lastname: Mihalj
authors.forename: Aleksandar
authors.initials: A
authors.lastname: Vcev
authors.forename: Johann
authors.initials: J
authors.lastname: Ennen
authors.forename: Arijan
authors.initials: A
authors.lastname: Tadzic
authors.forename: Ines
authors.initials: I
authors.lastname: Drenjancevic
mesh_terms: D000959:Antihypertensive Agents / Q000627:therapeutic use*; D062186:Arterial Pressure / Q000187:drug effects*; D040881:CD11a Antigen / Q000097:blood; D002121:Calcium Channel Blockers / Q000627:therapeutic use*; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D019040:E-Selectin / Q000097:blood; D004727:Endothelium / Q000378:metabolism; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000378:metabolism*; D039441:Integrin alpha4 / Q000097:blood; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D007958:Leukocyte Count; D007962:Leukocytes / Q000378:metabolism; D016256:Lewis X Antigen / Q000097:blood; D008024:Ligands; D008297:Male; D008875:Middle Aged; D009363:Neoplasm Proteins / Q000378:metabolism*; D011509:Proteoglycans / Q000378:metabolism*; D018401:Sample Size; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
chemical_list: D000959:Antihypertensive Agents; D040881:CD11a Antigen; D002121:Calcium Channel Blockers; D015815:Cell Adhesion Molecules; D019040:E-Selectin; C101134:ESM1 protein, human; D016256:Lewis X Antigen; D008024:Ligands; D009363:Neoplasm Proteins; D011509:Proteoglycans; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D039441:Integrin alpha4