title: Dissociation of left ventricular hypertrophy, beta-myosin heavy chain gene expression, and myosin isoform switch in rats after ascending aortic stenosis.
abstract: BACKGROUND
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Physiology, University of Heidelberg, Germany. rudolf.wiesner@urz.uni-heidelberg.de
authors.forename: R J
authors.initials: RJ
authors.lastname: Wiesner
authors.forename: H
authors.initials: H
authors.lastname: Ehmke
authors.forename: J
authors.initials: J
authors.lastname: Faulhaber
authors.forename: R
authors.initials: R
authors.lastname: Zak
authors.forename: J C
authors.initials: JC
authors.lastname: Rüegg
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001012:Aorta, Abdominal; D001013:Aorta, Thoracic; D001024:Aortic Valve Stenosis / Q000378:metabolism* / Q000503:physiopathology; D006332:Cardiomegaly / Q000378:metabolism / Q000503:physiopathology; D005260:Female; D006352:Heart Ventricles; D006439:Hemodynamics; D017379:Hypertrophy, Left Ventricular / Q000378:metabolism* / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism*; D018995:Myosin Heavy Chains / Q000096:biosynthesis*; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D014158:Transcription, Genetic
chemical_list: D012333:RNA, Messenger; D018995:Myosin Heavy Chains