Positive inotropic stimulation.

Abstract

Adrenergic receptors transduce signals through the G proteins to regulate cardiac function. The catecholamines, via alpha- and beta-adrenergic receptor (beta-AR) stimulation, may play a role in the development of heart failure. Norepinephrine and isoproterenol can induce cardiac myocyte apoptosis. Studies suggest that alpha-, beta1-, and beta2-adrenergic pathways differentially regulate cardiac myocyte apoptosis. The stimulation of beta1-AR leads to cyclic AMP-dependent apoptosis, whereas that of the beta2-AR elicits concurrent apoptosis and survival signals in cardiac myocytes coupled to Gs protein. Overexpression of alpha1-adrenergic receptors does not induce apoptosis in wild-type mice. In contrast, the heart failure observed in some murine models has to be related to an enhanced beta-AR kinase expression. These recent advances make it possible to understand the beneficial effects of beta-blockers in the treatment of chronic heart failure and provide novel therapeutic modalities through the stimulation of beta2-ARs or the inhibition of beta-AR kinase expression.

• Authors: Marc Leone, Jacques Albanèse, Claude Martin
• Journal: Current opinion in critical care (Curr Opin Crit Care) Vol. 8 Issue 5 Pg. 395-403 (Oct 2002) ISSN: 1070-5295 [Print] United States
• PMID: 12357106 (Publication Type: Journal Article, Review)

Chemical References

• Adrenergic beta-Antagonists
• Receptors, Adrenergic, beta
• Cyclic AMP-Dependent Protein Kinases
• beta-Adrenergic Receptor Kinases
• Isoproterenol

Topics

• Adrenergic beta-Antagonists (therapeutic use)
• Animals
• Apoptosis (drug effects)
• Cyclic AMP-Dependent Protein Kinases (antagonists & inhibitors)
• Humans
• Isoproterenol (therapeutic use)
• Mice
• Mice, Transgenic
• Myocytes, Cardiac (drug effects, metabolism)
• Receptors, Adrenergic, beta (drug effects, metabolism)
• Signal Transduction (drug effects)
• beta-Adrenergic Receptor Kinases