ABSTRACT
A critical site in the efferent sympathetic control is at the level of the β-adrenergic receptor, which plays a pivotal role in response to neural traffic and also to circulating catecholamines. Cardiac performance is modulated to an important extent by the adrenergic nervous system under baseline conditions, in response to stress and also in the presence of cardiovascular disease. The sarcolemmal fraction contains partially purified plasma membrane vesicles in which the adrenergic receptor density is more concentrated than in the crude pellet. The cardiomyopathic failing heart showed similar findings of decreased β-adrenergic receptor density and decreased adenylate cyclase responses to isoproterenol but normal forskolin responsiveness. One potential mechanism for the changes in the β-adrenergic receptor–adenylate cyclase complex in the failing heart involves desensitization, secondary to the chronic high levels of circulating catecholamines found in heart failure. Several studies have demonstrated major alterations in β-adrenergic receptor control in the presence of myocardial ischemia.
