Dissociation between factors resulting in hypertrophy and changes in myosin isoenzyme population of the pressure-loaded rat heart

  • H. Rupp
  • N. Popova
  • R. Jacob

Summary

The interrelationship between cardiac hypertrophy induced by increased pressure load and concomitant changes in the myoeardial myosin isoenzyme population was studied. In order to induce severe load on predominantly one ventricle, 6-week-old Wistar rats were fed on seeds of the plant Crotalaria spectabilis for 4 weeks. The ensuing pulmonary hypertension resulted in significant hypertrophy of only the right ventricle (52 %). In contrast, the isoenzyme population of myosin was affected in both ventricles, more so, however, in the right ventricle, as shown by the proportion of ventricular myosin (VM)-3 given as a percentage of the 3 ventricular myosin isoenzymes (right ventricle 29.7 ± 4.8 % VM-3 vs. 20.6 ± 5.3 % VM-3 of left ventricle; VM-3 of left and right ventricles of control rats was 9.3 ± 1.8%). Since thyroid hormones are major determinants of cardiac myosin isoenzymes and since Crotalaria spectabilis also affects other organs beside the lungs, serum thyroxine was determined. The thyroid hormone was significantly reduced, not, however, thyroxine binding index. The results suggest that reduced concentrations of circulating thyroid hormones contribute to the shift towards VM-3 in the myosin isoenzyme population. Since normal adult rats also exhibit an increased proportion of VM-3 in the predominantly loaded ventricle, it is concluded that beside the action of thyroid hormones, other mechanisms are responsible for the expression of the different myosin isoenzymes, such as those arising from altered adrenergic responsiveness and transmitter status of myocardium.

Key words

hypertrophy myosin isoenzymes Crotalaria spectabilis pulmonary hypertension thyroid hormones 

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Copyright information

© Dr. Dietrich Steinkopff Verlag, GmbH & Co. KG, Darmstadt 1983

Authors and Affiliations

  • H. Rupp
    • 1
  • N. Popova
    • 1
  • R. Jacob
    • 1
  1. 1.Physiologisches Institut IIUniversität TübingenTübingenGermany

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