Expression of β_2-Adrenergic Receptor and the Receptor Post Signaling Material in Myocardial Infarction Rats / 中国循环杂志

ABSTRACT

Objective:To investigate the mRNA expression of β_2-adrenergic receptor(β_2-AR) and the receptor post signaling materials cyclic AMP(cAMP) and cAMP-dependent protein kinase (PKA) activity in myocardial infarction(MI)rats.Methods:MI model was made by ligation of rats'left anterior descending coronary artery.A total of 48 adult Wistar rats were randomly divided into four groupsControl group,the rats were sham operated,and 2 weeks post MI group,4 weeks post MI group and 8 weeks post MI group.The myocytes suspensions were untreated or treated in each group by salbutamol,isoproterenol,ICI118,551,atenolol,propranolol and pertussis toxin(PTX)respectively.The mRNA expression of β_2-AR and β_1-AR from left ventricular myocardium were detected by RT-PCR,the concentration of cAMP was determined by competitive enzyme immunoassay and the activity of PKA was determined by non-radioactive protein kinase assay.Results:Compared with Control group,the mRNA expression of β_1-AR was lower in MI groups(P<0.05),and the ratio of β_2-AR to β-AR increased from 19% to 38%(P<0.01)after MI.Compared with the untreated cells,cAMP concentration was increased by salbutamol treatment in Control group and 2 weeks,4 weeks,8 weeks post MI group by 98.1%,133.6%,147.7% and 150.7% respectively(P<0.05).Compared with isoproterenol treatment,ICI118,551 decreased cAMP concentration in 8 weeks post MI group(P<0.05).Atenolol decreased cAMP in Control group,2 weeks and 4 weeks post MI groups(P<0.05);Propranolol decreased cAMP concentration in Control and three MI groups(P<0.05).β-receptor inhibitor inhibited PKA activity in 8 weeks post MI group(P<0.05),Atenolol inhibited PKA activity in Control group and 2 weeks post MI group(P<0.05),Propranolol inhibited PKA activity in Control group and three MI groups(P<0.05,respectively).Conclusion:The ratio of β_2-AR to β-AR increased after MI.β_2-AR agonist increased cAMP concentration and PKA activity in myocytes in post MI rats.