Effects Of TNF-αonβ3-adrenoreceptor Expressions Of Cardiac Myocyte In Vitro And Its Possible Mechanism

ObjectiveTumor necrosis factor-alpha expression andβ3-AR expression are upregulated during sepsis in the human myocardium and mediate an increased negative inotropic response. NO was similarly involved in the depressed myocardial responsiveness to catecholamines observed in patients with heart failure, a condition also associated with systemic inflammation. Therefore, Our present study is to investigate effects of TNF-αonβ3-AR expression of cardiac myocyte and its possible mechanism.MethodsUsing sterile technique, hearts from 2-days-old SD rat were removed, pooled, and minced into small blocks. The cells were disaggregated with pancreatic trypsin and collagenase. Suspensions were centrifuged and plated into the culture flask. Cells were incubated at 37℃in 5% CO2 and growth media was changed every 48 h. In fourth day, treatment of cardiomyocytes with TNF alpha and/or L-NAME, then demonstrate the presence ofβ3-AR both at the mRNA level and at the protein level with a specific monoclonal antibody.Results1.Below the concentration of 1.6ng/ml and before the time of 12 hours, TNF-alpha can cause a time-dependent and concentration-dependent increase inβ3-AR expression of cardiomyocytes.2.Treatment of cardiomyocytes with TNF alpha and L-NAME, L-NAME could diminishe but not abolishe the effect of TNF-alpha.ConclusionTreatment of cardiomyocytes with TNF-alpha caused a time-dependent and concentration-dependent increase inβ3-AR expression of cardiomyocytes, and the effect is diminished but not abolished by L-NAME. This change may contribute to cardiac dysfunction.