The Effects And Possible Mechanism Of (Beta(2)Ar Gene Expression In Cardiocytes Of Canines With Heart Failure

The objective of the present study was to observe the changes of beta(2)-adrenergic receptor (beta(2)AR) protein expression in a canine model of heart failure (HF), and the function of cardiocytes after transfection with Adv-beta(2)AR. The canine model of chronic HF was induced by rapid right ventricular pacing and cardiocytes were isolated with collagenase II. Cardiocytes were transfected with Adv-beta(2)AR to observe contractile function with a motion edge-detection system of single cells. Expression of (beta(2)AR protein in cardiocytes was measured by immunoblotting and the levels of intracellular cAMP were measured by ELISA. Compared with the control group (the sham group), the expression of beta(2)AR protein in HF cardiocytes did not change, but the basal (1 mM Ca2+) contraction amplitude percentage (1.809 +/- 0.922 vs. 1.120 +/- 0.432%, P<0.05), the maximum contraction amplitude percentage (14.855 +/- 2.377 vs. 10.784 +/- 2.675%, P<0.01) and the basal levels of intracellular cAMP (9.39 +/- 2.54 vs. 5.26 +/- 0.95 pmol/ml, n=6, P<0.05) of HF cardiocytes were significantly decreased. However, when HF cardiocytes were transfected with Adv-beta(2)AR and cultured for 48 h, compared with the non-transfected group, the basal contraction amplitude percentage (0.851 +/- 0.324 vs. 1.629 +/- 0.522%, P<0.05), the maximum contraction amplitude percentage (9.260 +/- 2.208% vs. 12.205 +/- 1.437%, P<0.01) and the basal levels of intracellular cAMP (5.26 +/- 0.95 vs. 9.03 +/- 1.03 pmol/ml, n=6, P<0.05) of cardiocytes in the transfected group were significantly increased. In conclusion, the expression of beta(2)AR protein in HF cardiocytes did not change, but contraction function was impaired. The moderate overexpression of beta(2)AR gene in the HF cardiocytes increased the levels of intracellular cAMP and improved contraction function.