title: Gene polymorphisms of endothelial nitric oxide synthase and angiotensin-converting enzyme in patients with asthma.
abstract: BACKGROUND
  Nitric oxide, including that produced by endothelial constitutive nitric oxide synthase (ecNOS), may regulate vascular and airway tone in the lungs and may influence various aspects of airway homeostasis. Angiotensin-converting enzyme (ACE) is expressed at high levels in the lungs and plays a role in the metabolism of angiotensin II, bradykinin, and substance P, all of which are potentially involved in the pathogenesis of asthma. An insertion-deletion polymorphism of the ACE gene has been shown to be associated with enzyme activity levels of ACE. To examine the possible involvement of the ecNOS and/or ACE genes as the genetic basis of bronchial asthma, we investigated whether there was any association between bronchial asthma and polymorphisms of the ecNOS and/or ACE genes.
  
  
  METHODS
  A total of 310 patients with bronchial asthma and 121 healthy subjects took part in this study. The ecNOS and ACE genotypes were determined in all subjects by polymerase chain reaction.
  
  
  RESULTS
  1) The distribution of one genotype (bb) of ecNOS was significantly higher in the asthma group than in the control population. 2) The ACE genotype distribution was not significantly different between the control and the asthma groups. 3) In asthmatic patients, the ACE and ecNOS genotype distribution did not differ significantly among groups of patients with different severities of asthma.
  
  
  CONCLUSIONS
  These results suggest that polymorphisms of the ecNOS gene, but not the ACE gene, may be associated with the development of asthma. However, the severity of asthma may not be influenced by polymorphisms of the ecNOS and ACE genes.
authors.affiliation: Department of Internal Medicine, Research Institute of Clinical Medicine, Chonbuk National University Medical School, Chonju, South Korea.
authors.forename: Y C
authors.initials: YC
authors.lastname: Lee
authors.forename: K T
authors.initials: KT
authors.lastname: Cheon
authors.forename: H B
authors.initials: HB
authors.lastname: Lee
authors.forename: W
authors.initials: W
authors.lastname: Kim
authors.forename: Y K
authors.initials: YK
authors.lastname: Rhee
authors.forename: D S
authors.initials: DS
authors.lastname: Kim
mesh_terms: D000328:Adult; D000368:Aged; D001249:Asthma / Q000201:enzymology / Q000235:genetics*; D004730:Endothelium, Vascular / Q000201:enzymology; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D008297:Male; D008875:Middle Aged; D019001:Nitric Oxide Synthase / Q000235:genetics*; D052250:Nitric Oxide Synthase Type III; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D012083:Renin / Q000235:genetics*; D012720:Severity of Illness Index
chemical_list: C496314:NOS3 protein, human; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III; D012083:Renin