title: Is there an association between angiotensin-converting enzyme gene polymorphism and functional activation of monocytes and macrophage in young patients with essential hypertension?
abstract: BACKGROUND
  This study was undertaken to determine whether the phenotype of monocytes and monocyte-derived macrophages is more proatherogenic in young persons with arterial hypertension and whether this phenotype is affected by smoking or polymorphism of the angiotensin-converting enzyme (ACE) gene.
  
  
  METHODS
  We enrolled 40 young patients (24.1 +/- 4.7 years) with previously untreated arterial hypertension and 40 age-matched healthy controls. There were 20 smokers and 20 non-smokers in each group.
  
  
  RESULTS
  In the hypertensive group, we found enhanced monocyte expression of CD11a (P < 0.001), reduced expression of CD49d (P < 0.001) and CD62L (P < 0.005), greater oxidative stress in resting and phorbol-12-mistrate-13-acetate-stimulated monocytes (P < 0.001), enhanced adhesion of monocytes to endothelial cells (P < 0.001), greater expression of CD36 on monocyte-derived macrophages (P < 0.001), and enhanced production of reactive oxygen species by resting and phorbol-12-mistrate-13-acetate-stimulated macrophages (P < 0.001). Cigarette smoking by hypertensive patients was associated with enhanced (P < 0.002) CD11a expression. There were no associations of ACE gene polymorphism with cellular expression or reactive oxygen species production studied among hypertensive patients. Only CD62L expression in DD homozygote participants was higher (P < 0.039) than in II homozygote participants.
  
  
  CONCLUSIONS
  It is concluded that arterial hypertension affects the function of monocytes/macrophages in young persons. Polymorphism of the ACE gene is without effect on the functional activation of monocytes and macrophages.
authors.affiliation: Department of Clinical Biochemistry and Laboratory Diagnostics, Pomeranian Medical University, Szczecin, Poland.
authors.forename: Danuta
authors.initials: D
authors.lastname: Zapolska-Downar
authors.forename: Aldona
authors.initials: A
authors.lastname: Siennicka
authors.forename: Kornel
authors.initials: K
authors.lastname: Chełstowski
authors.forename: Krystyna
authors.initials: K
authors.lastname: Widecka
authors.forename: Iwona
authors.initials: I
authors.lastname: Goracy
authors.forename: Maciej
authors.initials: M
authors.lastname: Hałasa
authors.forename: Bogusław
authors.initials: B
authors.lastname: Machaliński
authors.forename: Marek
authors.initials: M
authors.lastname: Naruszewicz
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000097:blood; D018955:CD36 Antigens / Q000096:biosynthesis; D016022:Case-Control Studies; D002448:Cell Adhesion; D042783:Endothelial Cells / Q000378:metabolism; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D006973:Hypertension / Q000235:genetics* / Q000378:metabolism* / Q000503:physiopathology; D039041:Integrin alpha4beta1 / Q000096:biosynthesis; D019041:L-Selectin / Q000096:biosynthesis; D016169:Lymphocyte Function-Associated Antigen-1 / Q000096:biosynthesis; D008264:Macrophages / Q000378:metabolism* / Q000502:physiology; D008297:Male; D009000:Monocytes / Q000378:metabolism* / Q000502:physiology; D018384:Oxidative Stress; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D010641:Phenotype; D011110:Polymorphism, Genetic; D017382:Reactive Oxygen Species / Q000378:metabolism; D012907:Smoking
chemical_list: D015415:Biomarkers; D018955:CD36 Antigens; D039041:Integrin alpha4beta1; D016169:Lymphocyte Function-Associated Antigen-1; D017382:Reactive Oxygen Species; D019041:L-Selectin; D007703:Peptidyl-Dipeptidase A