The coordinated, emergent regulation of nervous, endocrine, hemodynamic and metabolic processes in response to critical illness is characterized by marked release of catecholamines. Despite several-fold increases in circulating catecholamines, which correlate with clinical outcome, there is a limited understanding of the receptor and cellular consequences of this fundamental critical illness response. Beta-adrenoreceptors are pivotal in the response to this catecholamine surge, playing disparate roles in shaping physiological responses during different stages of critical illness. Here we review mechanisms and common disease processes through which acute and chronic alterations in β-adrenoreceptor physiology may affect important components of critical illness and discuss emerging therapeutic roles for beta-adrenoreceptor manipulation.
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