A. Busjahn et al., ANGIOTENSIN-CONVERTING ENZYME AND ANGIOTENSINOGEN GENE POLYMORPHISMS,PLASMA-LEVELS, CARDIAC DIMENSIONS - A TWIN STUDY, Hypertension, 29(1), 1997, pp. 165-170
We tested the hypotheses that angiotensin-converting enzyme insertion/
deletion (I/D) and angiotensinogen 235 methionine/threonine (M/T) subs
titution gene polymorphisms influence angiotensin-converting enzyme an
d angiotensinogen serum concentrations and cardiac dimensions in 91 mo
nozygotic and 41 dizygotic twin pairs. Cardiac dimensions were determi
ned echocardiographically. Angiotensin-converting enzyme levels were 2
4 +/- 11, 43 +/- 18, and 58 +/- 24 U/L for the II, ID, and DD genotype
s, respectively (P < .01). Posterior wall thickness was 8.1 +/- 1.3, 8
.6 +/- 1.7, and 8.9 +/- 1.9 mm for these genotypes (P < .05). Angioten
sin-converting enzyme levels were correlated with posterior wall thick
ness (r = .15, P < .05). The intrapair differences in angiotensin conv
erting enzyme levels for monozygotic, concordant dizygotic, and discor
dant dizygotic twins were 1.36 +/- 1.6, 1.86 +/- 1.6, and 17.25 +/- 4.
3 U/L, respectively. The angiotensinogen M/T genotypes exerted no infl
uence on cardiac dimensions or on angiotensinogen concentrations. The
additive genetic effect on angiotensin-converting enzyme levels (0.49)
, on posterior wall thickness (0.26), and on septum thickness (0.37) w
as significant (P < .01), although shared and nonshared environmental
effects were also identified. Our data confirm the impressive effect t
hat the angiotensin-converting enzyme D allele exerts on angiotensin-c
onverting enzyme plasma levels. Furthermore, our data also suggest tha
t the angiotensin-converting enzyme gene locus is primarily responsibl
e for angiotensin-converting enzyme plasma levels. Our twin study also
indicates that the angiotensin-converting enzyme gene locus is geneti
cally linked to posterior wall thickness. The correlation between angi
otensin-converting enzyme levels and posterior wall thickness suggests
that this effect is exerted by angiotensin-converting enzyme. We were
unable to demonstrate genetic linkage between the angiotensinogen gen
e locus and cardiac dimensions in this study.