Relationship between the Autoantibody and Expression of β(3)-Adrenoceptor in Lung and Heart

BACKGROUND: Evidences suggest that β(3) -adrenoceptor (β(3)-AR) plays an important role in heart failure (HF), although no data is reported indicating how these effects may change with the increasing age. Pulmonary congestion and edema are the major life-threatening complications associated with HF. The purpose of this study is to explore the relationship between the anti-β(3)-AR autoantibody and the expression of β(3)-AR in the lungs and heart for both aged patients and rats with HF. METHODS: Synthetic β(3)-AR peptides served as the target antigens in ELISA were used to screen the anti-β(3)-AR autoantibody in aged patients and rats. Two aged rat models were constructed based on aortic banding and sham-operation. The expression of β(3)-AR mRNA and protein in the lung and heart was measured in intervention and non-intervention groups by Western blot analysis at the baseline, 5(th), 7(th), 9(th) and 11(th) week, respectively. RESULTS: The frequency and titer of anti-β(3)-AR autoantibody in aged patients and rats with HF were higher than those in the control group (p<0.05). The expression of β(3)-AR mRNA and protein in pulmonary tissues decreased continually from the 7(th) week (p<0.05), followed by HF observed during the 9(th) week. The expression of β(3)-AR in myocardial tissues continued to increase after the 9(th) week (p<0.05), and the expression of both β(3)-AR mRNA and protein in the BRL group [HF group with BRL37344 (4-[-[2-hydroxy-(3-chlorophenyl)ethyl-amino] phenoxyacetic acid) (a β(3)-AR agonist) injection] was positively correlated with BRL37344 when compared with non-BRL group (HF group without BRL37344 injection) (p<0.05). CONCLUSION: Anti-β(3)-AR autoantibody was detected in aged patients and rats with HF. The expression of β(3)-AR mRNA and protein in pulmonary tissues decreased continually, and began earlier than in the heart, but its expression in myocardial tissues increased continually and could be further promoted by β(3)-AR agonist.