Jonggonnee WattanapermpoolTaneerath RiabroySurin PreawnimMahidol University2018-09-072018-09-071999-12-31Life Sciences. Vol.66, No.6 (1999), 533-543002432052-s2.0-0033621339https://repository.li.mahidol.ac.th/handle/20.500.14594/25776Our previous biochemical and mechanical studies have demonstrated an increase in Ca2+sensitivity of cardiac myofilaments in ovariectomized rats. To test whether the body weight gain associated with ovariectomy contributed some effects to the changes in myofibrillar functions, the relations of pCa (-log Ca2+molar concentration) to actomyosin adenosine triphosphatase (ATPase) activity of isolated myofibrillar preparations from 10-week pair-fed ovariectomized rats were compared with those from sham- operated controls. Despite similar body weights, the maximum myofibrillar ATPase activity was significantly lower in pair-fed ovariectomized rats as compared to that of sham-operated controls. In addition, the pCa-actomyosin ATPase relationship of pair-fed ovariectomized hearts still demonstrated a significant leftward shift in pCa50(-log half-maximally Ca2+activation) from that of sham-operated controls. To find out which hormone was responsible for the observed increase in myofibrillar Ca2+sensitivity, different sex hormone supplemental regimens were administered to ovariectomized rats. Subcutaneous injection of estrogen (5 μg/rat) or estrogen plus progesterone (1 mg/rat) three times a week could effectively prevent the changes in body weight, heart weight, and uterine weight of the ovariectomized animals. Moreover, supplements of either estrogen or progesterone could prevent a decrease in maximum ATPase activity. In contrast, only the estrogen replacement could abolish the Ca2+hypersensitivity of the myofilaments in these ovariectomized rats. These results suggest differential cardio-regulatory effects of ovarian sex hormones on the Ca2+activation of the myofilaments.Mahidol UniversityPharmacology, Toxicology and PharmaceuticsArticleSCOPUS10.1016/S0024-3205(99)00623-2