Influence of myocardial ischemia and reperfusion on beta-adrenoceptor subtype expression

The effects of ischemic injury and reperfusion on myocardial beta-adrenoceptor expression were examined in dogs after 30 min of left anterior descending coronary artery (LAD) ligation. Three sets of six dogs were allocated to either sham ligation (group I), 30 min ischemia without reperfusion (group II), or ischemia with 1 h of reperfusion (group III). The density of total beta-adrenoceptors along with beta1- and beta2-adrenoceptor subtypes were compared in tissue from the ischemic LAD and nonischemic left lateral zones by using radioligand binding with 125-labeled iodocyanopindolol (ICYP). In the control animals, there was no difference between total beta-adrenoceptors (43.8 +/- 7.2 vs. 40.7 +/- 8.0 fmol/mg protein +/- SEM) or percentage beta-adrenoceptor subtypes between the two zones. In group II, total beta-adrenoceptors increased 19.9% (p = 0.03) in the LAD compared with the lateral zone after 30 min of ischemia. Both beta-adrenoceptor subtypes increased, but only the increase in beta2-adrenoceptor was significant (39.8%; p = 0.02). Animals in group III revealed no difference in total beta-adrenoceptors density between LAD and lateral zones (48.3 +/- 13.4 vs. 55.2 +/- 8.5 fmol/mg protein). Brief myocardial ischemia is associated with an increase in total beta-adrenoceptors, attributed predominantly to increased beta2-adrenoceptors density. The increase in beta-adrenoceptor density is reversible after 1 h of reperfusion.