Effects of recombinant human brain natriuretic peptide on myocardial remodeling and connexin 43 expression in rats with heart failure

TAN Wenting; PENG Weirui; TANG Fen; LIU Shengquan; LONG Junrong; CHU Chun

doi:10.3969/j.issn.1002-266X.2017.33.003

Abstract：Objective To investigate the effects of recombinant human brain natriuretic peptide (rhBNP) on the myocardial remodeling and connexin 43 (Cx43) expression of rats with cardiac failure caused by pressure overload.Methods Forty-five male SD rats were randomly divided into the heart failure group (group F), heart failure+rhBNP group (group B), and sham operation group (group SO) with 15 rats in each group.In the group F and group B, we established the rat models of pressure overload-induced heart failure by abdominal aortic constriction, while in the SO group, rats did not receive coarctation of the abdominal aorta.Rats in the group B were subcutaneously injected with rhBNP (25 ug/kg/d), while rats in the group SO and group F were injected intraperitoneally with normal saline for 8 weeks.The left ventricular function, hemodynamics, QT dispersion, left ventricular myocardial pathology, myocardial fibrosis and collagen deposition, and myocardial Cx43 protein expression were detected in each group.Results Compared with the SO group, the left ventricular function, hemodynamics, QT dispersion, left ventricular myocardial histopathology, myocardial fibrosis deposition, myocardial Cx43 protein expression were statistically significant in the group F (all P<0.05), which showed that heart failure model was established successfully.Compared with group F, the heart function of rats increased, the mean arterial pressure and QT dispersion decreased, the disordered arrangement of myocardial cells reduced, collagen deposition decreased between cardiac myocytes, and the expression of Cx43 increased in the group B (all P<0.05).Conclusion rhBNP can improve the cardiac function and hemodynamic indexes in rats with heart failure under pressure overload, up-regulate the myocardial expression of Cx43 protein, and inhibit myocardial remodeling.