Expression of β1- and β2-adrenergic receptors in the lungs and changes in the levels of corresponding autoantibodies in an aged rat model of heart failure.

β-adrenergic receptors (β-ARs) and anti-β1-AR autoantibodies play important roles in heart failure. This study was designed to investigate the expression of β1- and β2-ARs in the lungs, and their relevance to the corresponding autoantibodies in an aged rat model of heart failure. In addition, we investigated the association between anti-β-AR autoantibody and soluble Fas (sFas) and soluble Fas ligand (sFasL). Aged male Wistar rats were divided into the sham-operated control group and the heart failure group. At 0 and 9 weeks post-surgery, the protein levels of β1- and β2-ARs in the heart and lungs were measured by western blot analysis. The plasma concentrations of autoantibodies, sFas and sFasL were determined by enzyme-linked immunosorbent assay (ELISA). The protein levels of pulmonary β1- and β2-ARs were decreased in the heart failure group when compared with the control group (P<0.01). Both the frequencies of the occurrence and the titers of autoantibodies against β2-AR increased at 9 weeks post-surgery (P<0.01). The levels of sFas and sFasL were also elevated, although there was no difference in the levels of sFas and sFasL between the groups, with positive and negative anti-β-AR autoantibody. These findings suggested that during the development of heart failure, the densities of pulmonary β1- and β2-ARs decreased. The levels of anti-β2-AR autoantibody exhibited similar changes as those of anti-β1-AR autoantibody, and there was no definite association between anti-β-AR autoantibody and the levels of sFas/sFasL.