Summary
The aim of our study was to analyse the mechanisms underlying cardiac toxicity caused by β-adrenoceptor stimulation and the relationships with their associated downregulation during heart failure. We used the experimental model of coronary artery ligation-induced myocardial infarction in male Wistar rats. In order to increase β-adrenergic stimulation, rats were subjected to a 15-day chronic isoprenaline administration (30 μg/kg/h). Isoprenaline administration induced haemodynamic inotropic compensation, almost abolished in vitro inotropic response to isoprenaline on papillary muscle (P
