Jonggonnee WattanapermpoolPeter J. ReiserMahidol UniversityOhio State University2018-09-072018-09-071999-08-01American Journal of Physiology - Heart and Circulatory Physiology. Vol.277, No.2 46-2 (1999)036361352-s2.0-0032869181https://repository.li.mahidol.ac.th/handle/20.500.14594/25332The 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.Mahidol UniversityBiochemistry, Genetics and Molecular BiologyMedicineArticleSCOPUS