scholarly journals The angiotensin-converting enzyme insertion/deletion polymorphism is associated with phagocytic NADPH oxidase-dependent superoxide generation: potential implication in hypertension

2010 ◽  
Vol 119 (4) ◽  
pp. 185-185
Author(s):  
G. San José ◽  
A. Fortuño ◽  
M. U. Moreno ◽  
P. A. Robador ◽  
J. Bidegain ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Nadph Oxidase ◽  
Converting Enzyme ◽  
Deletion Polymorphism ◽  
Superoxide Generation ◽  
Potential Implication

The angiotensin-converting enzyme insertion/deletion polymorphism is associated with phagocytic NADPH oxidase-dependent superoxide generation: potential implication in hypertension

2009 ◽  
Vol 116 (3) ◽  
pp. 233-240 ◽  
Author(s):  
Gorka San José ◽  
Ana Fortuño ◽  
María U. Moreno ◽  
Pablo A. Robador ◽  
Julen Bidegain ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Converting Enzyme ◽  
Nadph Oxidase ◽  
Plasma Levels ◽  
Converting Enzyme ◽  
Phagocytic Cells ◽  
Deletion Polymorphism ◽  
Potential Implication ◽  
Normotensive Subjects ◽  
O2 Production

The objective of the present study was to analyse the influence of the ACE (angiotensin-converting enzyme) gene I/D (insertion/deletion) polymorphism on NADPH oxidase-dependent O2•− (superoxide radical) production, and to investigate the clinical implication of this association in hypertensive subjects. A case-control study was performed in a random sample of the general population composed of 189 normotensive subjects and 223 hypertensive subjects. The ACE polymorphism was determined by PCR. NADPH oxidase-dependent O2•− production was quantified in phagocytic cells by chemiluminescence. MMP-9 (matrix metalloproteinase-9), a marker of atherosclerosis previously reported to be associated with NADPH oxidase overactivity, was quantified by ELISA in plasma samples. The distribution of genotypes was in Hardy–Weinberg equilibrium. The I/D polymorphism was not associated with hypertension. NADPH oxidase-dependent O2•− production was significantly higher in D/D (deletion/deletion) than in I/I (insertion/insertion) and I/D, both in normotensive and hypertensive subjects. Interestingly, plasma levels of angiotensin II were significantly higher in D/D than in I/I and I/D, both in normotensive and hypertensive subjects. Plasma levels of MMP-9 and systolic blood pressure values were significantly higher in D/D than in I/I and I/D hypertensive subjects, whereas no differences were found among genotypes in normotensive subjects. Interestingly, NADPH oxidase-dependent O2•− production positively associated with plasma MMP-9 levels in hypertensive subjects, which remained significant after adjustment for age and gender. In conclusion, in the present study we have reported for the first time an association of the D/D genotype of the ACE I/D polymorphism with phagocytic NADPH oxidase-mediated O2•− overproduction. Within the group of hypertensive patients, D/D cases also associated with increased blood pressure values and with enhanced plasma levels of MMP-9.

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