Density of adrenoceptors in rat heart and lymphocytes 48 hours and 7 days after acute myocardial infarction

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Abstract
Down regulation of the β adrenoceptor is thought to play an important role in the diminished response to catecholamines in heart failure. β Adrenoceptor densities were measured on membrane homogenates of rat right ventricle and lymphocytes 48 h or 7 d after experimental myocardial infarction, and in rats exposed to a continuous infusion of isoprenaline (400 μg·kg−1·h1). The performance of the rat hearts was also evaluated 48 h post infarction in an isolated retrograde perfused heart preparation. In contrast to a 60% down regulation in right ventricle and a 20% down regulation in lymphocyte membranes after isoprenaline infusion, there was no change in right ventricle and lymphocyte β adrenoceptor densities after myocardial infarction. Left ventricular contractile performance was significantly depressed 48 h after myocardial infarction. Mean basal left ventricular pressure decreased from 108(SEM 3) to 63(4) mm Hg while the maximal response to dobutamine was decreased from 204(4) to 105(12) mm Hg (n = 8). No correlation was found between the receptor densities of right ventricular and lymphocyte membranes. We conclude that diminished response to β sympathomimetics after myocardial infarction cannot be attributed to a loss of surface β adrenoceptors, and that the lymphocyte β adrenoceptor does not provide an adequate system to monitor small receptor changes on the myocardium.

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