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1 Department of Physiology, Faculty of Science, Mahidol University, Bangkok 10400, Thailand; and 2 Department of Oral Biology, College of Dentistry, Ohio State University, Columbus, Ohio 43210
The hypothesis
that ovarian sex hormone deficiency affects cardiac myofilament
activation was tested. Chemically skinned ventricular trabeculae and
single soleus muscle fibers were prepared from 10- and 14-wk
ovariectomized and control rats. Tension-pCa (
log [Ca2+]) relations of
left ventricular trabeculae and soleus fibers were compared to test
whether thin filament proteins are potential sites of modulated
activation. Trabeculae from ovariectomized rats exhibited a significant
increase in Ca2+ sensitivity with
no change in maximal tension-generating ability. In contrast, soleus
fibers demonstrated no shift in
Ca2+ sensitivity but generated
significantly less maximal tension. No changes in thin filament protein
isoform expression or loss of thin filament proteins were apparent in
the trabeculae or soleus fibers from ovariectomized rats. Although not
directly tested, our results are consistent with a possible modulation
of regulatory proteins (e.g., cardiac troponin I) to account for the
observed change in myofilament responsiveness of hearts from
ovariectomized rats. Other possible mechanisms for the altered
myocardial Ca2+ sensitivity after
ovariectomy are discussed.
myofilament calcium sensitivity; thin filament proteins; ovarian sex hormones
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