OBJECTIVE: To investigate the association between beta(3)-adrenergic receptor (beta(3)-AR) and oxidative stress in isoproterenol (ISO)-induced chronic heart failure (HF) rats. METHODS: Seven weight-matched normal adult rats (control), 18 ISO induced heart failure rats and 21 ISO induced heart failure rats treated with specific beta(3)-AR inhibitor, SR59230A for 6 weeks were included in this study. Echocardiography was performed at the end of the study and the myocardial levels of total superoxide dismutase (T-SOD) and lipid peroxidation (LPO) were measured by colorimetry, myocardial expression of beta(3)-AR was detected by reverse transcription-polymerase chain reaction (RT-PCR). RESULT: Compared with control group, the cardiac function was significantly reduced and myocardial beta(3)-AR mRNA expression was significantly increased, LPO level was also significantly enhanced while T-SOD level was significantly reduced in ISO group and these changes could be significantly attenuated by treatment with SR59230A. CONCLUSION: Our results showed that myocardial upregulation of beta(3)-AR is associated with increased oxidative stress in this model and beta(3)-AR inhibitor may be a new therapeutic agent for heart failure treatment.
OBJECTIVE: To investigate the association between beta(3)-adrenergic receptor (beta(3)-AR) and oxidative stress in isoproterenol (ISO)-induced chronic heart failure (HF) rats. METHODS: Seven weight-matched normal adult rats (control), 18 ISO induced heart failurerats and 21 ISO induced heart failurerats treated with specific beta(3)-AR inhibitor, SR59230A for 6 weeks were included in this study. Echocardiography was performed at the end of the study and the myocardial levels of total superoxide dismutase (T-SOD) and lipid peroxidation (LPO) were measured by colorimetry, myocardial expression of beta(3)-AR was detected by reverse transcription-polymerase chain reaction (RT-PCR). RESULT: Compared with control group, the cardiac function was significantly reduced and myocardial beta(3)-AR mRNA expression was significantly increased, LPO level was also significantly enhanced while T-SOD level was significantly reduced in ISO group and these changes could be significantly attenuated by treatment with SR59230A. CONCLUSION: Our results showed that myocardial upregulation of beta(3)-AR is associated with increased oxidative stress in this model and beta(3)-AR inhibitor may be a new therapeutic agent for heart failure treatment.
Authors: Rimantas Treinys; Danguolė Zablockaitė; Vida Gendvilienė; Jonas Jurevičius; V Arvydas Skeberdis Journal: J Membr Biol Date: 2014-02-15 Impact factor: 1.843
Authors: Vabren L Watts; Fernando M Sepulveda; Oscar H Cingolani; Alice S Ho; Xiaolin Niu; Rosa Kim; Karen L Miller; Koenraad Vandegaer; Djahida Bedja; Kathleen L Gabrielson; Gerald Rameau; Brian O'Rourke; David A Kass; Lili A Barouch Journal: J Mol Cell Cardiol Date: 2013-05-02 Impact factor: 5.000