Alterations of beta-adrenoceptors subsequent to myocardial infarction

Elevations and reductions of the number of beta-adrenoceptor binding sites are dependent on the strength and the duration of receptor interaction with respective agonists. In the paper presented here, results obtained by the authors concerning biosynthesis, storage and release of catecholamines following experimentally induced infarction of the myocardium in rats are compared with those of other authors for other species. Principally, storage and release of noradrenaline from ischemic hearts do not differ with the mode of inducing tissue hypoxia (stopped-flow ischemia, coronary artery ligation, occlusion of the great cardiac vein), nor for various species (rat, dog, guinea-pig). Differences are, however, present in the results of several beta-adrenoceptor binding studies performed after experimental myocardial infarction. Following acute infarction, an increase in the number of beta-adrenoceptor binding sites is generally observed, which is explained on the basis of an externalization of receptors from the cytoplasm ot the sarcolemmal membrane. Results pertaining to 2-3 days after infarction are not uniform: in guinea-pig hearts a marked drop in the number of beta-adrenoceptors has been reported, a mild rise in the number has been detected in the left and right ventricle of rat hearts. These divergent observations could arise from the experimental protocol employed, for instance in the binding assay and in the pretreatment given to the hearts prior to assay.