Hypertension, Vol 24, 30-36, Copyright © 1994 by American Heart Association
V Robert, N Van Thiem, SL Cheav, C Mouas, B Swynghedauw and C Delcayre
Cardiac fibrosis is one of the deleterious events accompanying hypertension
that may be implicated in the progression toward heart failure. To
determine the mechanisms involved in fibrosis and the role of hemodynamic
versus humoral factors, we studied the expression of genes involved in
hypertrophy and fibrosis in the heart of rats treated with aldosterone for
2 months with addition of 1% NaCl and 0.3% KCl in water. This treatment
induced arterial hypertension, a moderate left ventricular hypertrophy, and
a decrease in plasma thyroxine. Equatorial sections of hearts from treated
rats showed numerous foci of proliferating nonmuscular cells and a
biventricular fibrosis. Computerized videodensitometry demonstrated an
increase of collagen volume fraction by 152% and 146% and of the ratio of
the perivascular collagen area and vascular area by 86% and 167% in left
and right ventricles, respectively. As measured by slot blot, this cardiac
fibrosis was accompanied by an increase in alpha 1-I procollagen mRNA by
75% and 160% (P < .01) and in alpha 1-III mRNA by 76% and 319% (P <
.01) in left and right ventricles, respectively. Atrial natriuretic peptide
mRNA was induced only in the hypertrophied left ventricle. We conclude that
fibrosis is occurring and involves pretranslational regulation of collagen
synthesis. Whereas hypertrophy and atrial natriuretic peptide mRNA increase
are restricted to the left ventricle, fibrosis is initiated in both
ventricles, supporting the hypothesis that this cardiac response is
independent of hemodynamic factors.
ARTICLES
Increased cardiac types I and III collagen mRNAs in aldosterone-salt hypertension
INSERM U127, Hopital Lariboisiere, Paris, France.
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