Endothelial nitric oxide synthase gene Glu298Asp polymorphism and blood pressure, left ventricular mass and carotid artery atherosclerosis in a population-based cohort.
OBJECTIVE
Decreased production of endothelial nitric oxide (NO) is associated with different cardiovascular pathology. We studied the association between the Glu298Asp polymorphism of the NO producing gene, endothelial nitric oxide synthase (eNOS), and hypertension, left ventricular mass (LVM) and carotid artery intima-media thickness (IMT) in a population-based cohort of hypertensive and control subjects.


METHODS
Cross-sectional case-control study.


METHODS
District around Oulu University Hospital, Northern Finland.


METHODS
The study population consisted of 600 middle-aged hypertensive subjects (300 men and 300 women) and 600 controls (300 men and 300 women) living in the City of Oulu. The hypertensive subjects were randomly selected by age stratification from the Social Insurance Institute register for reimbursement of antihypertensive medication. For each hypertensive subject, an age- and sex-matched control was randomly selected from the national health register. The overall participation rate was 87.8%. In the present study a total of 1024 subjects were screened. Echocardiographic examinations were performed by a trained cardiologist and carotid ultrasonographic examinations by a trained radiologist.


RESULTS
The genotype distributions and allele frequencies between the hypertensive and control subjects and the relationship between the Glu298Asp variant and blood pressure, LVM and carotid artery IMT were determined. No differences in genotype distribution or allele frequencies were found between the hypertensive and control groups (the frequency of the Asp allele 0.299 vs. 0.288, respectively). Also, we could not find any association between the eNOS genotype and the measured cardiovascular complications.


CONCLUSIONS
The Glu298Asp variant of the eNOS gene does not seem to be a major risk factor for cardiovascular alterations in the general population.
Karvonen
J
J
Department of Internal Medicine, University of Oulu, Finland. jakarvon@paju.oulu.fi
Kauma
H
H
Kervinen
K
K
Rantala
M
M
Ikäheimo
M
M
Päivänsalo
M
M
Savolainen
M J
MJ
Kesäniemi
Y A
YA
D000483:Alleles; D001224:Aspartic Acid / Q000378:metabolism*; D001794:Blood Pressure / Q000235:genetics* / Q000502:physiology; D016893:Carotid Stenosis / Q000201:enzymology / Q000235:genetics*; D016022:Case-Control Studies; D015331:Cohort Studies; D003430:Cross-Sectional Studies; D004730:Endothelium, Vascular / Q000201:enzymology*; D005260:Female; D005387:Finland; D005787:Gene Frequency / Q000235:genetics; D005828:Genetics, Population; D005838:Genotype; D018698:Glutamic Acid / Q000235:genetics*; D006801:Humans; D006973:Hypertension / Q000201:enzymology / Q000235:genetics; D017379:Hypertrophy, Left Ventricular / Q000201:enzymology / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000235:genetics*; D011110:Polymorphism, Genetic / Q000235:genetics*; D012306:Risk
D001224:Aspartic Acid; D009569:Nitric Oxide; D018698:Glutamic Acid; D019001:Nitric Oxide Synthase