Author(s): Post SR, Hammond HK, Insel PA, Post SR, Hammond HK, Insel PA
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Abstract 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-adrenergic receptor pathways. Studies with failing hearts from humans and animals indicate 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 blunting 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 dysfunction. Even though this question remains unanswered, the concept of targeting the beta-adrenergic pathway in the failing heart is becoming increasing popular and several new therapeutic strategies are in development.
This article was published in Annu Rev Pharmacol Toxicol
and referenced in Cardiovascular Pharmacology: Open Access