title: Endothelial dysfunction in patients with asthma: the role of polymorphisms of ACE and endothelial NOS genes.
abstract: OBJECTIVE
  Polymorphisms of the angiotensin converting enzyme (ACE) and endothelial nitric oxide (eNOS) genes have been implicated in asthma pathogenesis. Angiotensin II and NO have important roles in maintaining vascular tone. In this study, the relationship between endothelial dysfunction and ACE and eNOS gene polymorphisms was investigated in patients with asthma.
  
  
  METHODS
  This cross-sectional, controlled study was conducted at the Yedikule Chest Disease Hospital and Cardiology Center in a University Hospital. Forty-nine patients with asthma (18 male, 31 female; mean age: 33+/-12 years) and 49 age- and sex-matched healthy controls (20 male, 29 female; mean age: 30+/-8 years) were included. Pulmonary function tests and flow-mediated dilatation of the brachial artery [endothelium dependent dilatation (EDD)] were examined by high-resolution ultrasonography. The ACE and eNOS genotypes were determined by PCR.
  
  
  RESULTS
  Asthma patients showed lower EDD (12+/-6% vs. 22+/-6%, p<0.001) as compared to controls. The EDD was correlated with both predicted value of FEV1 (r=0.31, p=0.04) and predicted value of FVC (r=0.37, p=0.013). Conversely, EDD values in patients with moderate asthma were significantly lower than those in patients with mild asthma (10.1+/-5.2% vs. 14.1+/-5.7%, p=0.017). However, the ACE and eNOS genotype distribution was not significantly different between controls and asthma groups. Furthermore, EDD was not associated with both gene polymorphism of ACE and eNOS.
  
  
  CONCLUSIONS
  Patients with asthma have decreased vasodilatatory response to shear stress (EDD). Decreased EDD is correlated with the severity of asthma, but not with the distribution of ACE and eNOS genotypes.
authors.affiliation: Pulmonary Medicine, Yedikule Chest Disease and Chest Surgery Hospital, Istanbul, Turkey. pinary70@hotmail.com
authors.forename: Pinar
authors.initials: P
authors.lastname: Yildiz
authors.forename: Huseyin
authors.initials: H
authors.lastname: Oflaz
authors.forename: Naci
authors.initials: N
authors.lastname: Cine
authors.forename: Hakan
authors.initials: H
authors.lastname: Genchallac
authors.forename: Nihan
authors.initials: N
authors.lastname: Erginel-Unaltuna
authors.forename: Alaattin
authors.initials: A
authors.lastname: Yildiz
authors.forename: Veysel
authors.initials: V
authors.lastname: Yilmaz
mesh_terms: D000328:Adult; D001249:Asthma / Q000235:genetics / Q000503:physiopathology*; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D005838:Genotype; D006801:Humans; D008297:Male; D019001:Nitric Oxide Synthase / Q000235:genetics*; D052250:Nitric Oxide Synthase Type III; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic; D012129:Respiratory Function Tests; D012720:Severity of Illness Index; D013314:Stress, Mechanical; D014664:Vasodilation
chemical_list: C496314:NOS3 protein, human; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III; D007703:Peptidyl-Dipeptidase A