Dissociation of left ventricular hypertrophy, β-myosin heavy chain gene expression, and myosin isoform switch in rats after ascending aortic stenosis

• Published in: Circulation (New York, N.Y.) N.Y.), 1997-03, Vol.95 (5), p.1253-1259
• Main Authors: WIESNER, R. J, EHMKE, H, FAULHABER, J, ZAK, R, RÜEGG, J. C
• Format: Article
• Language: English
• Subjects: Analysis of Variance; Animals; Aorta, Abdominal; Aorta, Thoracic; Aortic Valve Stenosis - metabolism; Aortic Valve Stenosis - physiopathology; Biological and medical sciences; Cardiology. Vascular system; Cardiomegaly - metabolism; Cardiomegaly - physiopathology; Female; Heart; Heart failure, cardiogenic pulmonary edema, cardiac enlargement; Heart Ventricles; Hemodynamics; Hypertrophy, Left Ventricular - metabolism; Hypertrophy, Left Ventricular - physiopathology; Medical sciences; Myocardium - metabolism; Myosin Heavy Chains - biosynthesis; Polymerase Chain Reaction; Rats; Rats, Sprague-Dawley; RNA, Messenger - biosynthesis; Transcription, Genetic
• ISSN: 0009-7322; 1524-4539
• DOI: 10.1161/01.CIR.95.5.1253

Reexpression of the fetal beta-myosin heavy chain (beta-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, beta-MHC gene expression was studied in an experimental model of pressure-over-load hypertrophy that is not associated with a concurrent activation of the circulating renin-angiotensin system. Hypertrophy was induced in rats by ascending aortic banding (n = 40). After 7 days, myosin contained 31% (P < .05) of the beta-MHC isoform in banded but < 5% in sham-operated animals. However, no specific elevation of beta-MHC mRNA levels was found in banded animals. In contrast, hearts of rats with abdominal aortic banding displayed a marked increase in beta-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. The results of the present work do not support the concept that increased beta-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 beta-MHC gene.