CARDIAC-FUNCTION IN GENETICALLY-ENGINEERED MICE WITH ALTERED ADRENERGIC-RECEPTOR SIGNALING

In disease states such as heart failure, catecholamines released from sympathetic nerve endings and the adrenal medulla play a central role in the adaptive and maladaptive physiological response to altered tiss ue perfusion. G protein-coupled receptors are importantly involved in myocardial growth and the regulation of contractility. The adrenergic receptors themselves are regulated by a set of specific kinases, terme d the G protein-coupled receptor kinases. The study of complex systems in vivo has recently been advanced by the development of transgenic a nd gene-targeted ''knockout'' mouse models. Combining transgenic techn ology with sophisticated physiological measurements of cardiac functio n is an extremely powerful strategy for studying the regulation of myo cardial contractility in normal animals and in models of disease state s. The purpose of this review is to summarize current knowledge about the regulation of cardiovascular homeostasis involving signaling pathw ays through stimulation of adrenergic receptors.