(Circulation. 1999;100:e85-e86.)
© 1999 American Heart Association, Inc.
Circulation Electronic Pages |
Department of Pharmacology Erasmus University Rotterdam, Rotterdam, The Netherlands
Klinik und Poliklinik für Innere Medizin II University of Regensburg, Regensburg, Germany
| Introduction |
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With great interest, we read the articles by O'Donnell et
al1 and Fornage et al2 in the May 12, 1998,
issue of Circulation. Their data suggest genetic linkage
between the ACE gene and blood pressure in men but not in women.
Likewise, we previously described associations of ACE with
arterial blood pressure3 and with ECG
evidence of left ventricular
hypertrophy4 only in men. It may be
worthwhile, therefore, to point to another apparent sexual dimorphism
of the renin-angiotensin system. In men, renin and prorenin
are
30% and 50% higher, respectively, than in women,5
a difference that may diminish during menopause. Renin is the second
major enzyme of this system and is responsible for generation of
angiotensin I (the substrate of ACE). It may thus be
speculated that men with genetically elevated ACE levels (DD
genotype) are confronted with higher angiotensin I
levels and, thereby, may have a higher chance to present with
complex phenotypes. The stoichiometry of ACE and renin was also
probed by a recent transgenic rat model with high levels of human ACE
transgene expression in the heart.6 Although this
transgenic animal has almost no apparent phenotype under
baseline conditions, abdominal aortic banding and subsequently high
renin levels resulted in enhanced left ventricular
hypertrophy. Similarly, Montgomery et al7
found a much more marked increase in left ventricular mass
in response to intense physical training in males with the ACE D
allele than in II homozygotes, whereas left ventricular
mass was similar in the genotype
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