(Circulation. 1997;95:1253-1259.)
© 1997 American Heart Association, Inc.
Articles |
Dissociation of Left Ventricular Hypertrophy, ß-Myosin Heavy Chain Gene Expression, and Myosin Isoform Switch in Rats After Ascending Aortic Stenosis
the Department of Physiology II (R.J.W., J.C.R.) and the Department of Physiology I (H.E., J.F.), University of Heidelberg (Germany), and the Department of Medicine (R.Z.), University of Chicago (Ill).
Correspondence to Dr Heimo Ehmke or Dr Rudolf J. Wiesner, Department of Physiology, University of Heidelberg, Im Neuenheimer Feld 326, 69120 Heidelberg, Germany. E-mail rudolf.wiesner@urz.uni-heidelberg.de or ehmke{at}novsrv1.pio1.uni-heidelberg.de
Background Reexpression of the fetal ß-myosin heavy chain (ß-MHC) gene was reported to be a marker for phenotypic reprogramming and cardiac hypertrophy in rats. Recent in vitro studies strongly suggested a role of angiotensin II for phenotypic reprogramming. In the present investigation, ß-MHC gene expression was studied in an experimental model of pressure-overload hypertrophy that is not associated with a concurrent activation of the circulating renin-angiotensin system.
Methods and Results Hypertrophy was induced in rats by ascending aortic banding (n=40). After 7 days, myosin contained 31% (P<.05) of the ß-MHC isoform in banded but <5% in sham-operated animals. However, no specific elevation of ß-MHC mRNA levels was found in banded animals. In contrast, hearts of rats with abdominal aortic banding displayed a marked increase in ß-MHC mRNA levels (3-fold to 5-fold, P<.05). Both the left ventricular weight and left ventricular peak systolic pressure were significantly elevated compared with sham-operated animals (abdominal aortic banding, +13% and 164±7 mm Hg; ascending aortic banding, +27% and 191±9 mm Hg). Plasma renin activity was elevated in rats with abdominal aortic banding (2.5-fold, P<.05) but not in rats with ascending aortic banding.
Conclusions The results of the present work do not support the concept that increased ß-MHC gene expression is a general "stable late marker" of myocardial hypertrophy in rats. Our results suggest that the stimulation of the renin-angiotensin system is crucial for the activation of the ß-MHC gene.
Key Words: angiotensin • blood pressure • hypertrophy • remodeling • stenosis
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