β-Adrenoceptor density in chronic infarcted myocardium: a subtype specific decrease of β1-adrenoceptor density

β-adrenoceptor density is altered in different cardiac diseases. In heart failure β-adrenoceptor density is down regulated but in acute myocardial ischemia β-adrenoceptor density is up regulated. In hearts with myocardial infarction total β-adrenoceptor density is decreased shortly after myocardial infarction. Aims and methods: To investigate whether total β-adrenoceptor number is altered in the chronic phase after myocardial infarction, and to identify the specificity of alteration, we studied male Wistar rats (n=18) which underwent a ligation of the left coronary artery or a sham operation. Twelve weeks after coronary ligation, rats were sacrificed and hearts were excised, perfused to obtain blood-free myocardium and frozen in liquid nitrogen. Infarcted myocardium was identified visually and separated from non-infarcted myocardium. Total β-adrenoceptor number was calculated in fmol (−)-[125I]iodocyanopindolol specifically bound/mg protein and the relative amount of β1- and β2-adrenoceptor density was measured by inhibition of (−)-[125I] iodocyanopindolol binding with CGP 20712 A. Results: Total β-adrenoceptor number in infarcted myocardium was significantly decreased (25.7±1.4 vs. 24.9±2.2 vs. 20.1±3.2 fmol/mg protein (P=0.03) resp. Sham vs. Non-infarcted vs. Infarcted myocardium), due to a decrease of only β1-adrenoceptor density (14.7±0.61 vs. 12.7±1.09 vs. 4.84±0.96 fmol/mg protein (P=0.004) resp.), whereas the β2-adrenoceptor density and the dissociation constant (Kd) were not significantly decreased. Conclusion: In the infarcted myocardium total β-adrenoceptor density is decreased due to a decreased β1-adrenoceptor density at 12 weeks after myocardial infarction.