Ariyaporn ThawornkaiwongSurin PreawnimJonggonnee WattanapermpoolMahidol University2018-07-242018-07-242003-03-07Life Sciences. Vol.72, No.16 (2003), 1813-1824002432052-s2.0-0037424330https://repository.li.mahidol.ac.th/handle/20.500.14594/20755Changes in cardiac myofilament Ca2+activation have been demonstrated in ovariectomized rats. The underlying mechanisms responsible for these changes, however, are unknown. Accordingly, we measured both density and binding affinity of cardiac β1-adrenergic receptors in sarcolemmal preparations from 10-week ovariectomized rats, pair-fed ovariectomized rats, and sham-operated control rats. Receptor protein content was also measured by immunoblotting. Deprivation of ovarian sex hormones for 10 weeks induced a significant upregulation of β1-adrenergic receptors without affecting binding affinity. The same magnitude of receptor upregulation was also detected in pair-fed ovariectomized hearts. To determine which hormone is responsible for the observed increase in β1-adrenergic receptor density, various sex hormone supplemental regimens were administered to ovariectomized rats. Subcutaneous injection of estrogen (5 μg/rat), progesterone (1 mg/rat), or estrogen plus progesterone three times a week all effectively prevented the upregulation of the β1-adrenoceptors. Western blot analyses using polyclonal antibody of β1-adrenergic receptors revealed the same pattern of changes in the protein content of the receptors in these various groups of experimental hearts as those obtained from the receptor binding assay. These results suggest a possible direct suppressive effect of ovarian sex hormones on the expression of cardiac β1-adrenergic receptors. © 2003 Elsevier Science Inc. All rights reserved.Mahidol UniversityBiochemistry, Genetics and Molecular BiologyPharmacology, Toxicology and PharmaceuticsArticleSCOPUS10.1016/S0024-3205(02)02473-6