Cardiac beta-adrenergic receptors, which respond to neuronally released and
circulating catecholamines, are important regulators of cardiac function.
Congestive heart failure, a common clinical condition, is associated with a
number of alterations in the activation and deactivation of beta-adrenergi
c receptor pathways. Studies with failing hearts from humans and animals in
dicate that such alterations include changes in the expression or function
of beta-adrenergic receptors, G-proteins, adenylyl cyclases, and G-protein
receptor kinases. The net effect of these alterations is the substantial bl
unting of beta-adrenergic receptor-mediated cardiac response. An important
unanswered question is whether the loss of cardiac beta-adrenergic receptor
responsiveness is a contributing cause, or a result, of ventricular dysfun
ction. Even though this question remains unanswered, the concept of targeti
ng the beta-adrenergic pathway in the failing heart is becoming increasingl
y popular and several new therapeutic strategies are in development.