Objective To observe the effects of β3-adrenergic receptor (β3-AR) antagonist on myocardial Uncoupling protein2 (UCP2) expression and energy metabolism in chronic heart failure rats.
Methods 7 weight-matched normal adult rats (control group), 18 rats with ISO induced heart failure (ISO group) and 21 rats with ISO induced heart failure but received specific β3-AR inhibitor SR59230A (ISO+ SR59230A group) for 6 weeks were included in this research. At the end of the study, Echocardiography was performed; the ratio of left ventricular weight and body weight (LVW/BW) was calculated. The expression of β3-AR and UCP2 mRNA in myocardium were detected by reverse transcription-polymerse chain reaction (RT-PCR), the UCP2 protein in myocardium were detected by western blot. The myocardial contents of creatine phosphate (PCr) and adenosine triphosphate (ATP) were measured by high performance liquid chromatography (HPLC).
Results Compared with control group, the cardic function was significantly reduced and myocardial β3-AR mRNA significantly increased, UCP2 mRNA and protein was also significantly increased in ISO group, this change could be attenuated by the treatment with SR59230A, and the expression of myocardial UCP2 protein negatively correlated with PCr contents.
Conclusions In the chronic stage of heart failure, the expression of UCP2 increases, which causes myocardial energy shortage, SR59230A improves myocardic energy efficiency and cardiac function by means of suppressing the the expression of UCP2.