Thyroid hormones (THs) enhance MHC alpha gene- and repress MHC beta 
gene-transcription in the heart, by interacting with specific nuclear receptors 
(TRs), that bind to regulatory sequences localized upstream of basal promoter of 
myosin heavy chain (MHC) genes. The overall effects of THs include an increase 
in V1- and a decrease in V3-myosin isozyme concentration in the heart. Myosin V1 
contains two MHC alpha chains and has a higher ATPase activity than V3 isoform, 
which contains two beta chains. Previous studies on papillary muscles of 
spontaneously hypertensive rats (SHRs) showed that heart hypertrophy is 
accompanied by a shift from alpha to beta MHC accumulation. The present study 
was aimed at evaluating whether this event relates to differential expression of 
alpha1, alpha2, and beta1 isoforms of TRs. At the ages of 8 and 15 weeks, SHRs 
and Harlan Sprague-Dawley control rats were sacrificed under anesthesia and 
their hearts were dissected into left and right ventricles, free of atria and 
great vessels. The results of Western blot analyses showed that the levels of 
the three TR isoforms do not differ significantly between SHRs and control rats 
of the same age, either in the left or in the right ventricle. Thus, the 
expression of MHC beta in SHR hypertrophic heart does not seem to depend on 
changes in TR isoform concentrations.